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Proteins are defying textbooks

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We bet this isn’t the only time they have done so. 😉

Here, from U Utah Healthcare:

Open any introductory biology textbook and one of the first things you’ll learn is that our DNA spells out the instructions for making proteins, tiny machines that do much of the work in our body’s cells. Results from a study published on Jan. 2 in Science defy textbook science, showing for the first time that the building blocks of a protein, called amino acids, can be assembled without blueprints – DNA and an intermediate template called messenger RNA (mRNA). A team of researchers has observed a case in which another protein specifies which amino acids are added.

“This surprising discovery reflects how incomplete our understanding of biology is,” says first author Peter Shen, Ph.D., a postdoctoral fellow in biochemistry at the University of Utah. “Nature is capable of more than we realize.”

To put the new finding into perspective, it might help to think of the cell as a well-run factory. Ribosomes are machines on a protein assembly line, linking together amino acids in an order specified by the genetic code. When something goes wrong, the ribosome can stall, and a quality control crew is summoned to the site. To clean up the mess, the ribosome is disassembled, the blueprint is discarded, and the partly made protein is recycled.

Yet this study reveals a surprising role for one member of the quality control team, a protein conserved from yeast to man named Rqc2. More.

But what is this about “Nature is capable of more than we realize”? Does nature have a mind that has a search space for solutions?

Like a half-made car with extra horns and wheels tacked to one end, a truncated protein with an apparently random sequence of alanines and threonines looks strange, and probably doesn’t work normally. But the nonsensical sequence likely serves specific purposes. The code could signal that the partial protein must be destroyed, or it could be part of a test to see whether the ribosome is working properly. Evidence suggests that either or both of these processes could be faulty in neurodegenerative diseases such as Alzheimer’s, Amyotrophic lateral sclerosis (ALS), or Huntington’s.

“There are many interesting implications of this work and none of them would have been possible if we didn’t follow our curiosity,” says Brandman. “The primary driver of discovery has been exploring what you see, and that’s what we did. There will never be a substitute for that.”

Are these people trying to say, don’t fire us because we find evidence for design in nature?

If so, let’s hope they are not forced to yelp some fake disclaimer at a press conference.

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255 Replies to “Proteins are defying textbooks

  1. 1
    mahuna says:

    Um, I wouldn’t start celebrating another Intelligent Design victory. You just admitted that amino acids can be assembled into genes without DNA or RNA existing first.

    I think this gives new life to the primordial soup.

    Of course we may simply be pushing the lump down the python. How did the first protein form, before it began assembling other proteins from raw amino acids? I mean, cells are formed by other cells, which are formed by genes which are formed by DNA which are formed by RNA which can be formed by proteins which are formed from amino acids, which are formed by… Cells?

    I’m also guessing that “assembler proteins” can each only assemble 1 type of protein, which again means that there is Information embedded in the protein. And the Information got there… how?

  2. 2
    ppolish says:

    Its soup not slop, Mahuna. Soup is designed, slop is not:) “Soup” and “souping up” (noun/verb) are design metaphors. Fine tuned both.

  3. 3
    ppolish says:

    On the one hand, Design in Nature is incredibly obvious. And on the other hand, incredibly deniable. Scientifically obvious and scientifically deniable.

    Why would Design be so obvious and yet so deniable?

  4. 4
    PaV says:

    I’ve looked at this article. The title is fairly over-hyped. From what I remember, they are some actual proteins that work with the mRNA to add one or several amino acids to the end of the string, usually when there is a problem of transcription. So you have “proteins” recruiting t-RNAs. IIRC, this is linked to an elimination system in the cell which destroys defective proteins.

    It is something completely beyond the central theory of molecular biology, but not as radical as the cover article makes you think.

    Nevertheless, population genetics takes another blow, though slight.

  5. 5
    gpuccio says:

    mahuna:

    I am afraid that this paper is no great help for protein first theories of OOL.

    The protein, Rqc2 (about 1000 AAs long), “simply” adds random sequences of two AAs (Alanine and Threonine) at the carboxy-terminal end of an incomplete protein in cases of “stalled translation”.

    The abstract:

    In Eukarya, stalled translation induces 40S dissociation and recruitment of the ribosome quality control complex (RQC) to the 60S subunit, which mediates nascent chain degradation. Here we report cryo–electron microscopy structures revealing that the RQC components Rqc2p (YPL009C/Tae2) and Ltn1p (YMR247C/Rkr1) bind to the 60S subunit at sites exposed after 40S dissociation, placing the Ltn1p RING (Really Interesting New Gene) domain near the exit channel and Rqc2p over the P-site transfer RNA (tRNA). We further demonstrate that Rqc2p recruits alanine- and threonine-charged tRNA to the A site and directs the elongation of nascent chains independently of mRNA or 40S subunits. Our work uncovers an unexpected mechanism of protein synthesis, in which a protein—not an mRNA—determines tRNA recruitment and the tagging of nascent chains with carboxy-terminal Ala and Thr extensions (“CAT tails”).

    And from the article:

    “Yet this study reveals a surprising role for one member of the quality control team, a protein conserved from yeast to man named Rqc2. Before the incomplete protein is recycled, Rqc2 prompts the ribosomes to add just two amino acids (of a total of 20) – alanine and threonine – over and over, and in any order. Think of an auto assembly line that keeps going despite having lost its instructions. It picks up what it can and slaps it on: horn-wheel-wheel-horn-wheel-wheel-wheel-wheel-horn.”

    Emphasis mine.

    And:

    “Like a half-made car with extra horns and wheels tacked to one end, a truncated protein with an apparently random sequence of alanines and threonines looks strange, and probably doesn’t work normally. But the nonsensical sequence likely serves specific purposes. The code could signal that the partial protein must be destroyed, or it could be part of a test to see whether the ribosome is working properly. Evidence suggests that either or both of these processes could be faulty in neurodegenerative diseases such as Alzheimer’s, Amyotrophic lateral sclerosis (ALS), or Huntington’s.”

    Again, emphasis mine.

    So, no specific information added here by the protein, except for a “signal” that means: this is a defective protein.

    So, proteins remain incapable of generating sequence information, but they can certainly add functional signals, which can be recognized in a complex, integrated system.

    Not good for “proteins first” OOL theories.

    Very good for ID.

  6. 6
    Andre says:

    If I’m not mistaken, I think this is exactly what Dr. Wells predicted.

  7. 7
    wd400 says:

    I think you are probably mistaken, Andre. Citation?

  8. 8
    Dionisio says:

    So, no specific information added here by the protein, except for a “signal” that means: this is a defective protein.

    So, proteins remain incapable of generating sequence information, but they can certainly add functional signals, which can be recognized in a complex, integrated system.

    Not good for “proteins first” OOL theories.

    Very good for ID.

    As usually, gpuccio clarifies the problem for the confused interlocutors and the rest of us.
    🙂

    However, I have a question about this part of the text:

    Before the incomplete protein is recycled, Rqc2 prompts the ribosomes to add just two amino acids (of a total of 20) – alanine and threonine – over and over, and in any order.r

    How does Rqc2 do the ‘prompting’ ?
    Under what conditions?

  9. 9
    AVS says:

    So Gpuc, a signal that says “this is a defective protein,” doesn’t qualify as information?

  10. 10
    Andre says:

    I was not mistaken

    http://www.uncommondescent.com.....ical-form/

    The new research

    A team of researchers has observed a case in which another protein specifies which amino acids are added.

    Dr. Wells

    Even after RNAs are translated into proteins, the latter change in ways that cannot be traced back to DNA sequences.

  11. 11
    gpuccio says:

    AVS:

    “So Gpuc, a signal that says “this is a defective protein,” doesn’t qualify as information?”

    My statement was:

    “So, no specific information added here by the protein, except for a “signal” that means: this is a defective protein.”

    Emphasis added.

    The meaning is rather obvious:

    No information specific to generate a functional sequence is provided, but information is added in the form of a signal that the protein is not working. The signal is always the same (a random tail of alanine and threonine), and has a functional meaning (it marks the protein and its state), but is not a specific functional sequence for that specific protein. IOWs, it is not a substitute of mRNA, as mahuna seemed to believe.

    Satisfied?

  12. 12
    gpuccio says:

    Dionisio:

    The paper is not free, so I have no access to details. However, if you look at the picture in the reviewing article, it seems that the protein links the tRNAs for alanine and threonine, and then binds the ribosome and adds those aminoacids to the incomplete protein. IOWs, it acts like a mRNA, but has no specific sequence information, and can add only alanine and threonine.

  13. 13
    gpuccio says:

    Dionisio:

    Ah, the “condition” seems to be “stalled translation”, but it is not clear how that recruits the protein and its action.

  14. 14
    AVS says:

    So no information, except for the signal, and the signal is a random sequence of alanines and threonines. How can you say there is no sequence information then? Your argument sounds like doublespeak to me, are you a lawyer?

  15. 15
    gpuccio says:

    AVS:

    I am not a lawyer, but certainly you are one who does not want to understand.

    The “random sequence of alanines and threonines” is a signal, and it conveys information. But the information is always the same. It is information about the state of the protein (failed). It is information that has function only because it is recognized in the system by something else (that’s why I call it a “signal”).

    On the other hand, the specific sequence in each protein is functional because it confers a specific biochemical configuration and activity, which is different for each protein.

    mRNA conveys specific information for its protein, deriving it from the protein gene. Rqc2 does nothing like that. It marks different defective proteins with the same signal: “defective”. Is that the same thing for you?

    mahuna seemed to believe that the Rqc2 protein assembled specific proteins and conveyed the information for their sequence, like mRNA. I have only tried to correct that misunderstanding.

    However, maybe I can apply for law school, after all… 🙂

  16. 16
    AVS says:

    “It is information that has function only because it is recognized in the system by something else”
    This is how all molecular biology works.
    This signal I’m sure also has a specific configuration and activity.
    Genes produce the same functional effect as does this random sequence of alanines and theonines.
    And Rqc2 certainly does carry out a role similar to that of mRNA, it acts as a template for the addition of alanines and threonines which have a specific cellular function.

  17. 17
    Joe says:

    This is how all molecular biology works.

    Because it was intelligently designed to work like that/

  18. 18
    AVS says:

    That’s nice joe.
    You must be the center of attention at the kool-aid jug, huh?
    Let me know when you have something intelligent to say.
    I won’t hold my breath.

  19. 19
    Dionisio says:

    gpuccio @ 11

    This may be disappointing, but some of your interlocutors may never be satisfied with your explanations, no matter how clearly you write them. But many anonymous readers most probably enjoy reading your posts. Also presumably most commenters in this site enjoy your insightful posts, although quite often you explain complex issues that are above my pay grade. 🙂

  20. 20
    Dionisio says:

    gpuccio @ 12

    I think I understood your clear explanation. Thank you!

  21. 21
    Dionisio says:

    gpuccio @ 13

    I see what you mean. Thank you!

    Can’t wait to see more details about those intriguing ‘trigger’ mechanisms that are not so clear yet.

    There seem to be many of those hidden wonders referenced in peer-reviewed research papers these days, but maybe that’s just my biased misperception? 🙂

  22. 22
    Dionisio says:

    gpuccio @ 15

    maybe I can apply for law school, after all… 🙂

    Most probably you would do very well in law school too, but I’m sure many of us in this site would ‘selfishly’ prefer that you remain writing your insightful posts on the ‘intriguing’ issues revealed by the latest research papers in biology. 🙂

    It’s well known that ‘not wanting to understand’ is a much worse condition than ‘not being able to understand’. You have patiently tried to explain things over and over again to some interlocutors that appear to be in the former case.
    But the rest of us benefit from that effort you’ve made and the time you have spent writing your posts. Thank you.

  23. 23
    wd400 says:

    I’m afriad Andre @ 10, you are mistaken.

    A prediction is a statement about something that will happen in the future. In that passage Wells is just discussing (and misrepresenting) the many forms of post-transcriptional and post-translation modification that are already known.

    Moreover, simply adding random tails to stalled proteins isn’t creating a biologically important sequence at all, and presumably marks the peptide for destruction. So I don’t think it’s true that “DNA doesn’t code for the final structure of proteins” here, in any meaningful sense anyway.

  24. 24
    Joe says:

    Well DNA doesn’t code for the proteins’ functional shape. What’s the issue?

  25. 25
    Joe says:

    LoL! @ AVS- It looks like you did hold your breath for too long and on too many occasions. Let us know when unguided evolution has something and yes, we won’t be holding our breath for that one.

  26. 26
    gpuccio says:

    AVS:

    It’s not worth the while, however…

    This signal I’m sure also has a specific configuration and activity.

    No, it is clearly stated in the article that:

    ” Before the incomplete protein is recycled, Rqc2 prompts the ribosomes to add just two amino acids (of a total of 20) – alanine and threonine – over and over, and in any order. ”

    IOWs, the protein-ribosome complex can only add either alanine or threonine, and does so randomly.

    Obviously, there must be some other system which recognizes a random alanine-threonine tail (which in itself is extremely unlikely in a functional protein) as a marker of defective translation. That’s not because a random alanine threonine tail has a special biochemical activity, but because it is a signal which is recognized as a symbolic marker of the failure of translation.

    And Rqc2 certainly does carry out a role similar to that of mRNA, it acts as a template for the addition of alanines and threonines which have a specific cellular function.

    No, there is no template. The protein can only bind tRNAs of alanine and threonine, and conveys them randomly to the existing, defective protein to generate the tail. That is not a sequence template, like in mRNA, where each codon corresponds to an aminoacid in a symbolic code.

    Nucleic acids are molecule with a symbolic meaning in their sequence. The activity of this protein is conditioned only but its biochemical affinities, like any other effector molecule. It carries no symbolic template. Would you say that an enzyme “acts as a template” for the result of the reaction it catalyzes?

    I think you understand that: you are not stupid, after all. But for some reason you want to insist in your position. Your choice.

  27. 27
    AVS says:

    Yes, I can read, the complex adds alanines and threonines randomly. What I’m saying is that these sequences likely form a specific structural configuration and therefore activity. This activity certainly is biochemical in nature and is known to activate the heat shock response.

    If there was no template, as you say, then no amino acids would be added, or any of the 20 would be added, your choice. The Rqc2 protein is not a typical template in the sense that DNA and RNA are, but it certainly serves a very similar purpose.

    The “symbolic meaning” of each nucleotide in a nucleic acid is to match up with the correct binding partner; a process that is completely controlled by biochemical affinities. Which you’ll notice, by your own definition, is the exact same way that Rqc2 functions. Rqc2 and tRNA have specific sites that bind, functioning as a template for the addition of alanine and threonine just as mRNA and tRNA have specific binding sites during normal protein synthesis.

  28. 28
    Andre says:

    WD400

    Geez, it is really OK to concede a point, Darwin will not condenm you to heaven if you fail him, I promise, Dr. Wells made it clear that something other than RNA or DNA changes the protein, he said he suspected it was the protein itself, thus this paper vindicates his prediction.

    You win some you lose some WD400…..

  29. 29
    hrun0815 says:

    Andre, I believe that the modification of proteins by something other than RNA or DNA was reported in the fifties (it’s called phosphorylation). So unless Wells was making his statements significantly earlier than I suspect he was, he was not actually making any predictions. He was simply stating scientifically known facts.

    It appears that you are mistaken after all, yet you are unwilling to entertain the possibility that you are ignorant of the facts. Why is that?

  30. 30
    wd400 says:

    If there was a point to concede I’d happily do so. But it’s perfectly obvious that Wells isn’t making a prediction in that passage, it starts “We have rigorous experimental evidence that…”, i.e. it as already known. In fact, it has been known for decades that proteins modify other proteins, and that those modifying proteins are encoded by DNA.

  31. 31
    hrun0815 says:

    And of course there are many others like ubiquitination, methylation, acetylation, … And of course these modifications are performed by other proteins and alter the function of the modified protein.

    And there is even another DNA/RNA independent type of protein modification know, not one that adds or removes bits of the protein, but changes the folding of the protein. For example heat shock proteins can stabilize or refold proteins so they can regain or maintain their functions.

    Again, it is surprising that in a point where you are obviously in error, you’d rather stick to your guns than admit that you had made a mistake and Wells didn’t actually make such predictions.

  32. 32
    gpuccio says:

    AVS:

    “What I’m saying is that these sequences likely form a specific structural configuration and therefore activity. This activity certainly is biochemical in nature and is known to activate the heat shock response.”

    Any molecule has its configuration, and some chemical activity. That’s not the same thing as a protein, like an enzyme, which has a functional configuration which can accomplish a specific task.

    An epitope has its configuration and “activity”, but it acts as allergenic because it is recognized by the immune system. In itself, the epitope has no specific function. It is recognized as a marker of some external structure, and therefore the immune system reacts to it in a programmed way.

    An enzyme catalyzes a reaction.

    The two concepts are not the same.

    No one is denying that the “abnormal” tail is recognized because of its chemical configuration (or lack of configuration). But that configuration has the only purpose of marking the defective protein, in a system which is prepared to react to that signal.

    “The “symbolic meaning” of each nucleotide in a nucleic acid is to match up with the correct binding partner; a process that is completely controlled by biochemical affinities.”

    No. This is a common mistake. The coupling of the codon and the aminoacid is completely symbolic. The coupling is implemented by biochemical affinities, not controlled by them. See later.

    “Which you’ll notice, by your own definition, is the exact same way that Rqc2 functions.”

    No. Rqc2 can bimd the tRNA of alanine and threonine. There is no symbolic coupling here. See later.

    “Rqc2 and tRNA have specific sites that bind, functioning as a template for the addition of alanine and threonine just as mRNA and tRNA have specific binding sites during normal protein synthesis.”

    No. It is completely different. The protein binds a specific tRNA (well, two specific tRNAs), which are coupled to their specific AAs.

    mRNA binds the specific codons corresponding to the sequence in the mRNA, according to a biochemical activity bewteen nucleotides which is organized in a symbolic correspondence to AAs. The symbolic coupling is realized by the 20 tRNA aminoacyl synthetases, and has nothing to do with the biochemical reactions between nucleotides.

    Each mRNA bears a specific symbolic sequence, which is recognized by each tRNA and implements the correct sequence of AAs. Nucleic acids act as a substrate where a symbolic sequence is written, and the sequence itself has nothing to do with biochemical reactions. In that sense, they are a template for the final AA sequence. The same symbolic sequence is written in the DNA gene, transcribed in the mRNA, and translated in the protein.

    Nothing like that happens in the Rqc2 protein. The protein has no sequence written in itself. It generates random sequences with all the tRNAs it can recognize. It can recognize only two of them, so the random sequences are made of two AAs. If it could recognize all 20 tRNAs, the random sequences would be made of all AAs. That is not a symbolic template of a sequence. It is only a biochemical constraint which limits the outcome of a reaction. They are two completely different things.

    The reason why nucleic acids can convey information is that they have a sequence of nucleotides which can be used to write a symbolic sequence for a proteic chain by a symbolic code. Proteins are effector, but they cannot transmit their sequences to another protein. IOWs, they cannoy convey their information. That’s why “proteins first” theories of OOL have been largely abandoned, in favor of the myth of RNA world. RNA is the only known natural molecule which can act both as an effector and a template of symbolic information.

  33. 33
    AVS says:

    Before I even respond to that steaming pile, Gpuc, just answer this question:

    How are the CAT signal we’ve been talking about and the signal sequence that targets proteins to the ER any different?
    (Besides the fact that one is coded within the genome and the other is not)

  34. 34
    Joe says:

    Can unguided evolution account for proteins? No

    Can unguided evolution account for the DNA that encodes for amino acid sequences? No

    Can unguided evolution account for any signal sequence that targets proteins? No

    Look, people, just because we can observe and explain something doesn’t mean the blind watchmaker didit.

    “Oh noes, we understand how the process works therefor unguided evolution”- Really?

  35. 35
    Andre says:

    Right

    Either you guys are wilfully obtuse or just don’t understand.

    I’m not arguing about proteins, DNA or anything you think I am…..

    I’m only pointing out that Dr. Wells predicted that Proteins have the ability to do their own changes without any “blueprint” that neither uses RNA or DNA, this paper confirms that.

    That is all I’m saying but the scientists of this study must have been liars for Jesus when they said;

    Open any introductory biology textbook and one of the first things you’ll learn is that our DNA spells out the instructions for making proteins, tiny machines that do much of the work in our body’s cells. Results from a study published on Jan. 2 in Science defy textbook science, showing for the first time that the building blocks of a protein, called amino acids, can be assembled without blueprints – DNA and an intermediate template called messenger RNA (mRNA). A team of researchers has observed a case in which another protein specifies which amino acids are added.

    Wonder what “showing for the first time” means? O Yes that means Dr. Wells predicted it before it was shown and then they showed for the FIRST time that it does!

    They must be liars for Jesus? No? Or Dr. Wells must be some demon spawn from Hell that took a lucky guess right?

    Ahh I forgot your entire faith system is based on chance and luck, how silly of me to doubt your religion!

    How does your religion go? Just refresh our memories….. Does chance just need some time or do we give time a chance?

  36. 36
    wd400 says:

    You really ought to read what Wells said, and then what this paper says, and then perhaps look up the definition of “predicted” if you still think you are right after that.

    Its perfectly obvious that Wells is talking about well established modifications like glycosylation, and not predicting the addition of amino acids (the hint here is that we talks about glycosylation but not amino acids and cites papers describing the process…).

    You got it wrong, maintaining otherwise while spitting these insults is just silly.

  37. 37
    Andre says:

    WD400

    Again, I’m not arguing about that! Are you really that obtuse? I’m saying this!

    Dr. Wells predicted that Proteins does not need , RNA or DNA.

    This paper confirms that! Seriously dude to be all up in arms about it won’t change what I’m saying, the researchers said and what Dr. Wells said.

  38. 38
    Andre says:

    To clarify this for you,

    Dr Wells said;

    So DNA does not completely specify proteins;

    Even after RNAs are translated into proteins, the latter change in ways that cannot be traced back to DNA sequences.

    What the researchers said;

    The new finding goes against dogma, showing for the first time that the building blocks of a protein, called amino acids, can be assembled by another protein, and without genetic instructions

    Geez one of them must be a liar! Or? Are these researchers and Dr. Wells saying different things?

    Are they saying different things WD400?

    So do you still want to argue or do you get the point I’ve been trying to make? Surely my understanding of the English language is not that terrible?

  39. 39
    wd400 says:

    In afraid you ability to comprehend English is indeed “that bad”. There if no prediction in Wells’ passage, just a description of one class of modification that proteins undergo after they are produced, and a citation to a paper on that topic that predates this latest paper by more than a decade.

    This new paper describes another modification made to (growing) proteins: the addition of amino acids that marks a stalled protein for destruction. This modification is the only new thing in the paper, and nothing in the linked text refers to that.

    There’s no prediction. The new finding in this paper is not mentioned. The process that is mentioned has been known for decades.

    I don’t see how this could be made clearer…

  40. 40
    Andre says:

    Wd400

    So when they say for the first time, They are factually incorrect? Should you not contact them about their error? And Dr. Wells predicting that It’s not about DNA and RNA only has been known for decades?

    Or you can actually stop this silly game, and concede…..

    P.S. Not holding my breath, being condemned to heaven clearly petrifies you……

  41. 41
    gpuccio says:

    AVS:

    “How are the CAT signal we’ve been talking about and the signal sequence that targets proteins to the ER any different? (Besides the fact that one is coded within the genome and the other is not)”

    They are different because the signal sequence is a specific sequence which follows specific information about the position of AAs, while in the CAT the sequence is random, and only the composition of the sequence is constrained to two specific AAs.

    As we don’t know how the CAT signal is recognized, we can imagine that the nature of its recognition is more generic that the recognition of specific signal sequence, but we will be able to say more when we know the details.

    Another important difference is that the signal sequence is coded in the genome, while the CAT sequence is not coded at all: what is coded in the genome is simply the information for a protein which does what it does (Rqc2).

    So, to sum up:

    1) For protein signal sequences, we have a specific sequence, which is symbolically coded in the genome, then transcribed, then translated.

    2) The CAT sequence is not specific in its sequence (it varies randomly), and is only specific in its limited AA composition. Moreover, the observed sequences are not coded anywhere, but arise randomly each time.

    Now you can respond to my “steaming pile”, I suppose.

  42. 42
    wd400 says:

    Andre, please read more carefully, it might save you from embarrassing yourself further.

  43. 43
    hrun0815 says:

    Wow, the DK-effect is strong with this one.

    Andre, they are talking about two different things.

    Wells says something that has been known for over 60 years: DNA does not completely specify proteins. (For example, there are many modifications of proteins, performed by other proteins, that alter both their structure and function.)

    The paper says something that is new: Amino-acids can be added to a protein without being encoded by DNA/RNA.

    These two things are clearly not identical. So both statements are correct. Well’s statement is not a prediction, but rather an acknowledgement of decades-old research. And the paper found indeed a new modification.

  44. 44
    AVS says:

    Nope. Wrong gpuc. The signal sequence is not a single specific sequence. For a given protein it may be, but not when comparing different proteins with a signal sequence. An that’s the important part. The sequence does not matter, it only has to be mostly made up of hydrophobic amino acids. This is how the CAT sequence works, sequence does not matter, only the presence of specific amino acids. I can “imagine” that there is no functional difference between these two signaling sequences, the only difference is how they get there.

    I think it’s this basic misunderstanding in the changing importance of sequence vs. structure information in biology that is keeping you from comprehending what is really going on here.

  45. 45
    gpuccio says:

    AVS:

    Wrong. Each signal sequence has a specific sequence, which is coded in its gene. It is true that they are generally made up prevalently of hydrophobic aminoacids, but there is much more to them, as you can see from this quote from Wikipedia:

    “The core of the signal peptide contains a long stretch of hydrophobic amino acids that has a tendency to form a single alpha-helix. In addition, many signal peptides begin with a short positively charged stretch of amino acids, which may help to enforce proper topology of the polypeptide during translocation by what is known as the positive-inside rule.[3] At the end of the signal peptide there is typically a stretch of amino acids that is recognized and cleaved by signal peptidase. However this cleavage site is absent from transmembrane-domains that serve as signal peptides, which are sometimes referred to as signal anchor sequences. Signal peptidase may cleave either during or after completion of translocation to generate a free signal peptide and a mature protein. The free signal peptides are then digested by specific proteases.”

    That different sequences may have similar structure and function is well known. That does not mean that the sequence is useless, and that only the type of aminoacids is important.

    The fact remains that signal sequences are encoded and translated, while the CAT tails are random sequences generated without any specific sequence information, and with the only restraint of the two available aminoacids.

    I don’t understand why you want to deny such obvious facts. The protein adds two aminoacids randomly. That is completely different from the translation of an encoded sequence. Therefore, the protein is different from mRNA. That is simply obvious.

    What is your interest in such an obstinate denial? Are you trying a revival of a proteins first OOL theory, based on complex proteins which, by linking to the ribosome (OK, that would be proteins first with ribosomes…), can generate random proteins from a limited set of AAs? Is that your idea? Are you such a fool?

  46. 46
    AVS says:

    Saying each signal sequence has a specific sequence is the same as saying that each finished CAT sequence has a specific sequence. In both peptides, the exact sequence does not matter, it is the overall structure and biochemical properties that matter. There is no specific sequence motif for either. In fact, there’s a pretty good chance that the CAT tails form an alpha helix as well.

    And now we bring up the variations of the signal sequence in a huge wiki quote, great.
    We are talking about the ability of the signal sequence to localize the nascent chain to the ER, the short positively charged stretch is for proteins that remain embedded in the membrane and the cleavage sight some proteins have is unimportant to this discussion.

    I am not denying the fact that the signal sequence is encoded in the genome and the CAT sequence is not (I said this in post 33).

    If you don’t think that Rqc2 doesn’t serve some form of a template function than you are simply being stubborn. The CAT tails are not “generated without any sequence information,” the sequence information is in the Rqc2 protein and its addition of only two amino acids. This means the sequence will be made up only of these two residues and is analogous to the random, yet largely hydrophobic, sequence in signal peptides.

    I am in no way interested in a proteins first revival I am just trying to sort out your original statement that there is “no specific information added here by the protein, except for a “signal” that means: this is a defective protein.”
    Because, in fact, the protein in question does add specific information; the information necessary to activate the heat shock response, and it does so by adding a random sequence made up of two amino acids.
    Is the fact that this random sequence has a functional effect, what you don’t like?

  47. 47
    Andre says:

    WD400

    For the last time, I’m not arguing about what they do, I’m saying Dr. Wells said that proteins did not need blueprints for final form or function, these researchers showed it for the first time.

    Get it?

    Good!

  48. 48
    hrun0815 says:

    Andre, these researchers did not show, nor did they claim to show “that proteins did not need blueprints for final form or function” FOR THE FIRST TIME.

    They’d be idiots if they did since this fact has been known for over sixty years. even a high school student who took biology is probably aware of this. Try and figure out what they actually claim to have shown FOR THE FIRST TIME.

    You are displaying a bizarre mixture of the Dunning-Kruger effect, the inability to read accurately what they are claiming, and a pigheaded stubbornness.

  49. 49
    gpuccio says:

    AVS:

    Just to be clear:

    “If you don’t think that Rqc2 doesn’t serve some form of a template function than you are simply being stubborn.”

    It depends only on what you mean by “some form of template function”, which seems to be a very vague definition. If you mean only that the protein constrains the sequence to two aminoacids, and attachs it in the right place and to the right protein, that is certainly true. My point is only that in no way it determines the exact final sequence, like mRNA does. Which is certainly true.

    “The CAT tails are not “generated without any sequence information,” the sequence information is in the Rqc2 protein and its addition of only two amino acids. This means the sequence will be made up only of these two residues..”

    Whoever denied that?

    “…and is analogous to the random, yet largely hydrophobic, sequence in signal peptides.”

    This is false. In what sense is it similar? OK, they are made of aminoacids. Alanine is hydrophobic, but threonine is polar. And the sequence in signal peptides is not random at all. Where did you take that strange idea? The sequence is exactly coded in the genes. Are you saying that the genes are random?

    Moreover, your assumption that the sequence specificity in signal peptides is completely useless, and that any bunch of “largely idrophobic” aminoacids will do the trick is completely gratuitous and unwarranted.

    “Because, in fact, the protein in question does add specific information; the information necessary to activate the heat shock response, and it does so by adding a random sequence made up of two amino acids.
    Is the fact that this random sequence has a functional effect, what you don’t like?”

    Absolutely not! Why should I “not like” that simple fact? Of course the protein is adding specific information. Whoever denied that? However, protein is not adding specific sequence information, like the mRNA. This is the difference.

    So, it seems that we absolutely agree that the protein adds information, in the form of the constraint to those two aminoacids, and in the form of the correct attachment of such a signal to the right protein, so that it may be recognized. How can you think that I don’t like that concept, when I stated clearly from the beginning (post #5):

    “So, no specific information added here by the protein, except for a “signal” that means: this is a defective protein.”

    What is not clear in the word “except”?

    Why in the world do you think that I don’t like the idea that a random CAT tail, made of the right two aminoacids, and attached at the right target, is not information? Who called that a “signal”?

    My point is simply, and always has been, that there is no coded information for a specific sequence that guides the activity of the Rqc2 protein. That activity is only constrained by what the protein can do, and the protein acts always in the same way, so that the differences in the final CAT tails are random. Whatever system has to recognize that signal, must recognize that type of signal.

    My point is simply, and always has been, that mRNA is all another thing, because it conveys information for an exact sequence, an information which is symbolically coded and therefore transmittable in the genes, while the Rqc2 protein does nothing like that.

    My point is simply, and always has been, that they are two completely different things, and that mahuna was expressing a misleading concept when he said:

    “You just admitted that amino acids can be assembled into genes without DNA or RNA existing first.”

    (emphasis added)

    The working of the Rqc2 protein has nothing to do with genes and with heritable information (except, again, for the information in the protein structure itself, which obviously comes from a gene, and was translated by an mRNA).

  50. 50
    Andre says:

    hrun0815

    Riiiggght

    you said;

    Andre, these researchers did not show, nor did they claim to show “that proteins did not need blueprints for final form or function” FOR THE FIRST TIME.

    When they say………. and I quote!

    Open any introductory biology textbook and one of the first things you’ll learn is that our DNA spells out the instructions for making proteins, tiny machines that do much of the work in our body’s cells. Results from a study published on Jan. 2 in Science defy textbook science, showing for the first time that the building blocks of a protein, called amino acids, can be assembled without blueprints

    They are liars for Jesus then?

  51. 51
    hrun0815 says:

    Andre, this is my last reply to you. You are willfully ignorant, stubborn, unable to read but convinced that you are smart and knowledgable.

    “proteins did not need blueprints for final form or function”

    is not the same as

    “the building blocks of a protein, called amino acids, can be assembled without blueprints”

  52. 52
    Andre says:

    Please do pray tell how that makes a difference to what I’ve been trying to say about Dr Wells predicting it and these researchers confirming it?

    I’m curious……

  53. 53
    Joe says:

    Protein function and final form is fully determined by the sequence of constituent amino acids (whether the protein was translated from mRNA, synthesized in vitro or from random assembly)

    That is incorrect. Genetic engineers have spliced coding sequences into foreign hosts with very little success- that is only a few sequences actually made it to a functioning protein with most failing to find a functional form. Dr Sermonti mentions this in “Why Is a Fly Not A Horse?”

    Leaving aside chaperones, the sequence determines the folding and any enzymic activity or other useful property that protein might have.

    LoL! As if we can “leave aside chaperones” which help facilitate the folding of long polypeptides.

  54. 54
    Andre says:

    hrun015

    So final form and assembled is not the same thing?

    Assembled

    fit together the separate component parts of (a machine or other object).
    “my new machine is being assembled and my old one dismantled”

    synonyms: construct, build, fabricate, manufacture, erect, set up, join up, fit together, put together, piece together, connect, join, unite, patch up, sew (up)
    “how to assemble the kite”

    So saying final form is not the same as assembled? Is that what you’re arguing about?

  55. 55
    hrun0815 says:

    Somebody else try. I give up. If the earlier posts were not sufficient to explain it then I doubt anything I post from now on will do the trick.

  56. 56
    Joe says:

    Are you claiming chaperones can change the properties of a protein rather than facilitate folding and prevent tangling?

    How did you get that from what I posted?

    Regarding the way a protein molecule is synthesised, you must think sodium chloride from natural sea salt differs in chemical properties from that made in a lab.

    Obviously you are deluded.

    Strange that you can’t actually make a case and have to rely on innuendo based on your misconceptions.

  57. 57
    Joe says:

    So when you wrote “that is incorrect” what were you referring to?

    LoL! I was referring to what you wrote and I explained it. Did you not understand what I posted- the part after “That is incorrect”?

  58. 58
    Joe says:

    Genetic engineers have taken the genes that encode for functional proteins in one organism and spliced them into another species only to observe the resulting polypeptide not take shape and function. Dr Sermonti mentions this in the book “Why Is A Fly Not A Horse?”. If the protein’s shape was determined by the AA sequence that should not happen.

  59. 59
    Joe says:

    But that has nothing to do with the point that a particular amino acid sequence at a particular pH and temperature will fold to a particular conformation,

    It won’t/ may not fold at all and I never said chaperones add function.

  60. 60
    Joe says:

    Prions are proteins that when they contact another (sister) protein they change its shape. That shouldn’t be able to happen if the AA sequence determines the shape.

  61. 61
    Joe says:

    You’re mixed up between genes and proteins.

    No

    Genes may code for proteins.

    Yes

    Splicing in genes is a way of producing proteins.

    Some work while most do not form.

    Insulin is produced industrially using genetically engineered bacteria.

    Yes, insulin is one of the few that worked. Most others did not.

    I see you googled Anfinen’s dogma.

    Nope, you see something that never happened.

  62. 62
    Joe says:

    AGAIN:

    Genetic engineers have taken the genes that encode for functional proteins in one organism and spliced them into another species only to observe the resulting polypeptide not take shape and function. Dr Sermonti mentions this in the book “Why Is A Fly Not A Horse?”. If the protein’s shape was determined by the AA sequence that should not happen.

  63. 63
    Joe says:

    In vitro protein synthesis is routine.

    OK. What does that have to do with what I said? Dr Sermonti wasn’t talking about ALL proteins. The proteins that require chaperones, which are the bulk of proteins used in/by organisms, won’t find a functional shape without those chaperones.

    Human insulin is what, 51 amino acids- it doesn’t need any help to fold. Long proteins- amino acid wise- are the norm. They do not play by your rules.

  64. 64
    Joe says:

    What is the largest that blind and unguided processes are known to produce- that is without a cell nor its machinery? 😛

    Yarus, et al., did some work in that regard- what did they achieve?

    And how would you get from a small protein that doesn’t require any help to larger proteins that do? You just can’t keep adding on to a functional sequence like it’s a stalagmite.

  65. 65
    Joe says:

    So no answers to my questions, then- got it

  66. 66
    Eugen says:

    Aurelio
    “Sermonti must be 94.Perhaps he’s not familiar with the current state of affairs in commercial biochemistry…”

    Darwin would be 209, yet people use him as great authority. Imagine how much his ideas are far removed of the modern affairs in science.

  67. 67
    wd400 says:

    Darwin would be 209, yet people use him as great authority…

    [citation needed].

    Many of Darwins ideas are indeed removed from modern science, which kind of proves the point that he’s not considered an authority. Only those bits of Darwin’s thinking supported by subsequent science are part of today’s evolutionary biology. (We talk about natural selection, we don’t talk about pangenes).

  68. 68
    Joe says:

    Aurelio Smith- Am I supposed to guess the relevance of your links? Could you please make a case so it can be scrutinized?

    Just occurs to me, Joe. How is it possible to crystallise proteins (as was done to elucidate the 3D structure of haemoglobin using X-ray crystallography) if they need chaperones to fold consistently?

    Just occurs to me, Aurelio. Why don’t you respond to what I actually post instead of what you think I posted? Why can’t scientists crystallize proteins that they remove from live hosts?

  69. 69
    hrun0815 says:

    Why can’t scientists crystallize proteins that they remove from live hosts?

    And more DK-effects here.

    Mammalian proteins that are crystallized are generally not expressed in their native host tissue. Currently, the vast majority of crystallized proteins are expressed in bacteria. In cases where bacteria do not express the protein correctly, insect cell suspensions are generally the next best option.

    Also, Joe, since you suggest that it is not, in fact, amino-acid sequence that generally determines protein structure and function, is it your contention that a protein with the same sequence in two different organisms has in fact a different structure and/or function in these two organisms?

  70. 70
    Joe says:

    Mammalian proteins that are crystallized are generally not expressed in their native host tissue

    And?

    Currently, the vast majority of crystallized proteins are expressed in bacteria. In cases where bacteria do not express the protein correctly, insect cell suspensions are generally the next best option.

    OK so that supports what I thought- bacteria and insects are live hosts. Aurelio thinks they are synthesized.

    Also, Joe, since you suggest that it is not, in fact, amino-acid sequence that generally determines protein structure and function,

    1- It isn’t just me. There are papers that discuss the improbability of predicting a protein’s shape given its amino acid sequence.

    2- “generally determines” is too broad.

    is it your contention that a protein with the same sequence in two different organisms has in fact a different structure and/or function in these two organisms?

    No

  71. 71
    Dionisio says:

    #78 Aurelio Smith

    Can a document with over half of the authors from Hispanic background be reliable?

    🙂

  72. 72
    hrun0815 says:

    Joe earlier:

    Genetic engineers have taken the genes that encode for functional proteins in one organism and spliced them into another species only to observe the resulting polypeptide not take shape and function.

    Joe when confronted with the fact that in general mammalian proteins are expressed in bacteria to be crystallized in order to examine their native structure and with it their function:

    OK so that supports what I thought…

  73. 73
    hrun0815 says:

    Oh, and by the way:

    There are papers that discuss the improbability of predicting a protein’s shape given its amino acid sequence.

    is not equivalent to claiming that the amino acid sequence does not determine the protein’s structure or function.

  74. 74
    AVS says:

    Gpuc, I’m glad you have changed your mind, from “No, there is no template” to “there is at least some form of template function.”

    “My point is only that in no way it determines the exact final sequence, like mRNA does.”
    What would you say determines the final sequence of the CAT tail then?

    The sequence in a single specific signal peptide is not random; obviously it is encoded in the original gene. But there is no specific sequence of signal peptides; they are random in the same sense that the sequence of alanine and threonine are random in the CAT tail. The only thing that matters is hydrophobic content and formation of an alpha helix in the signal peptide versus alanine-threonine content and a likely alpha helix structure as well in the CAT tail.

    “your assumption that the sequence specificity in signal peptides is completely useless, and that any bunch of “largely hydrophobic” amino acids will do the trick is completely gratuitous and unwarranted.”
    No, it is completely true. There is no specific sequence motif associated with the signal peptide. Its only requirement is a hydrophobic stretch of amino acids, it can be of different length and sequence.

    “However, protein is not adding specific sequence information, like the mRNA.”
    mRNA and the Rqc2 protein direct the addition of very specific amino acids. mRNA does so, according to association with tRNA molelcues as does Rqc2. They perform the same function, but in different ways.

    “So, no specific information added here by the protein, except for a “signal” that means: this is a defective protein.”
    Is the equivalent of saying “I never get into car accidents, except for when I get into a car accident”
    That’s the lawyer doublespeak you seem to do so well.

    “while the Rqc2 protein does nothing like that,” “they are two completely different things.”
    But they do very similar things. It’s not an exact sequence, but Rqc2 produces a peptide that results in a specific function. They are very similar.

    Yes mahuna was off the mark with that statement. Way off.

  75. 75
    gpuccio says:

    AVS:

    Well, at least we agree on something at last.

    I don’t agree that “The only thing that matters is hydrophobic content”. Have you evidence of that?

    I don’t know where you get the “likely alpha helix structure as well in the CAT tail” concept.

    However, nothing of that is really important.

    I don’t understand why you say:

    “So, no specific information added here by the protein, except for a “signal” that means: this is a defective protein.”
    Is the equivalent of saying “I never get into car accidents, except for when I get into a car accident”
    That’s the lawyer doublespeak you seem to do so well.

    Maybe my English is really poor, but I believed that saying:

    “no specific information added except for a signal that means so and so”

    simply means that the signal information is added, and no other information. Is that doublespeak? The example of accidents is not appropriate. The protein could well add the information which represents the signal (a random sequence of alanine and threonine) and other information, for example a specific sequence with some other biochemical activity. So, I believe that my statement has a very clear meaning, and is not doublespeak. You are free to believe differently.

    However, I still consider the lawyer matter as a strange form of compliment. 🙂

    Deciding how similar the two things are, at this point, is a very subjective issue. I will be happy to keep my opinion, and to respect yours.

    And I am happy that you agree that mahuna was off the mark. Which was the only motivation of my initial post.

  76. 76
    Dionisio says:

    #91 gpuccio

    “no specific information added except for a signal that means so and so”

    simply means that the signal information is added, and no other information.

    Is that doublespeak?

    No. That’s clearspeak. 🙂

  77. 77
    AVS says:

    Gpuc, an unbroken stretch of hydrophobic residues is absolutely required, besides that there is little similarity between signal peptides. In fact, this is what makes predicting signal sequences very difficult. You can attach any random hydrophobic sequence that is about 6-15 residues long, to a cytosolic protein and it will be transported to the ER. These studies have already been done.

    The alpha-helix structure thing was a guess on my part, although it doesn’t really matter whether it’s a helix, a beta-sheet, whatever; the most important thing is that it makes some kind of structure that is recognized by HSP1, which apparently it does.

    The absolute clearest way to say it would have been “it adds the specific information that activates the heat shock response.” I don’t see any need for the “no specific information” part unless you are trying to lighten the blow in the fact that this protein creates a random sequence that adds information.
    It adds specific information, so the phrase “no specific information added” should not be in the sentence. But that’s just my opinion, although I do pride myself on saying exactly what I mean and meaning exactly what I say. =)

    You obviously aren’t aware of the attitude toward lawyers here in the US of A, it’s not a compliment.
    Ever heard of the phrase “ambulance chasers” or seen Breaking Bad?

    And Dio, you don’t know your rear-end from a hole in the ground, so I wouldn’t try to judge the clarity of someone’s words or open my mouth at all, if I were you.

    =)

  78. 78
    Dionisio says:

    Structural basis for translational surveillance by the large ribosomal subunit-associated protein quality control complex.

    doi: 10.1073/pnas.1413882111

    All organisms have […] mechanisms to manage the stalling of ribosomes upon translation of aberrant mRNA.

    In eukaryotes, the large ribosomal subunit-associated quality control complex (RQC), composed of the listerin/Ltn1 E3 ubiquitin ligase and cofactors, mediates the ubiquitylation and extraction of ribosome-stalled nascent polypeptide chains for proteasomal degradation.

    How RQC recognizes stalled ribosomes and performs its functions has not been understood.

    Using single-particle cryoelectron microscopy, we have determined the structure of the RQC complex bound to stalled 60S ribosomal subunits.

    The structure establishes how Ltn1 associates with the large ribosomal subunit and properly positions its E3-catalytic RING domain to mediate nascent chain ubiquitylation.

    The structure also reveals that a distinguishing feature of stalled 60S particles is an exposed, nascent chain-conjugated tRNA, and that the Tae2 subunit of RQC, which facilitates Ltn1 binding, is responsible for selective recognition of stalled 60S subunits.

    RQC components are engaged in interactions across a large span of the 60S subunit surface, connecting the tRNA in the peptidyl transferase center to the distally located nascent chain tunnel exit.

    This work provides insights into a mechanism linking translation and protein degradation that targets defective proteins immediately after synthesis, while ignoring nascent chains in normally translating ribosomes.

    http://www.ncbi.nlm.nih.gov/pubmed/25349383

  79. 79
    Dionisio says:

    Protein synthesis. Rqc2p and 60S ribosomal subunits mediate mRNA-independent elongation of nascent chains.

    doi: 10.1126/science.1259724.

    In Eukarya, stalled translation induces 40S dissociation and recruitment of the ribosome quality control complex (RQC) to the 60S subunit, which mediates nascent chain degradation.

    Here we report cryo-electron microscopy structures revealing that the RQC components Rqc2p (YPL009C/Tae2) and Ltn1p (YMR247C/Rkr1) bind to the 60S subunit at sites exposed after 40S dissociation, placing the Ltn1p RING (Really Interesting New Gene) domain near the exit channel and Rqc2p over the P-site transfer RNA (tRNA).

    We further demonstrate that Rqc2p recruits alanine- and threonine-charged tRNA to the A site and directs the elongation of nascent chains independently of mRNA or 40S subunits.

    Our work uncovers an unexpected mechanism of protein synthesis, in which a protein–not an mRNA–determines tRNA recruitment and the tagging of nascent chains with carboxy-terminal Ala and Thr extensions (“CAT tails”).

    http://www.ncbi.nlm.nih.gov/pubmed/25554787

  80. 80
    Dionisio says:

    Reconstitution of a minimal ribosome-associated ubiquitination pathway with purified factors.

    doi: 10.1016/j.molcel.2014.07.006.

    Ribosomes stalled on aberrant mRNAs engage quality control mechanisms that degrade the partially translated nascent polypeptide.

    Ubiquitination of the nascent protein is mediated by the E3 ligase Listerin via a mechanism involving ribosome subunit dissociation.

    Here, we reconstitute ribosome-associated ubiquitination with purified factors to define the minimal components and essential steps in this process.

    We find that the primary role of the ribosome splitting factors Hbs1, Pelota, and ABCE1 is to permit Listerin access to the nascent chain.

    Listerin alone can discriminate 60S- from 80S-nascent chain complexes to selectively ubiquitinate the former.

    Splitting factors can be bypassed by artificially removing the 40S subunit, suggesting that mere steric hindrance impedes Listerin recruitment.

    This was illustrated by a cryo-EM reconstruction of the 60S-Listerin complex that identifies a binding interface that clashes with the 40S ribosomal subunit.

    These results reveal the mechanistic logic of the core steps in a ribosome-associated quality control pathway.

    http://www.ncbi.nlm.nih.gov/pubmed/25132172

  81. 81
    gpuccio says:

    AVS:

    Thank you for the comments. You are entitled to judging my communication style as you like. I will go on trying to communicate as I think is correct.

    However, please believe (if you want) that there was never in my mind any intention or desire to “lighten the blow in the fact that this protein creates a random sequence that adds information”, for the very simple reason that, IMHO, that is not a blow at all.

    I see no problem at all in the fact that it is possible to add functional information by creating a random sequence in a controlled context.

    My only intention (believe it or not) was to clarify the differences between what happens in this context and what happens in mRNA directed protein synthesis, because at the beginning of this thread there seemed to be great confusion about that.

    In Italy, lawyers are not exactly considered so bad as they are in the USA, but maybe we can catch up, if we really try. 🙂

    However, I always enjoyed this old joke:

    A physician, an engineer, and an attorney were discussing who among them belonged to the oldest of the three professions represented. The physician said, “Remember, on the sixth day God took a rib from Adam and fashioned Eve, making him the first surgeon. Therefore, medicine is the oldest profession.”

    The engineer replied, “But, before that, God created the heavens and earth from chaos, and thus he was the first engineer. Therefore, engineering is an older profession than medicine.”

    Then, the lawyer spoke up. “Yes,” he said, “But who do you think created chaos?”

  82. 82
    Dionisio says:

    gpuccio

    Your statement quoted in post #92 seems correct to me.

    The way you used the conjunction ‘except’ before a statement that indicated the only thing that was not included in or referred to by the preceding statement, seems very clear to me.

    For example, the statement “I don’t want to drink anything, except water” is as clear as water. 🙂

    I’d suggest you refrain from discussing anything with interlocutors (specially the ones across the ocean) who may not know the correct meaning and use of certain words. 🙂

    For example, some folks in that part of the world can’t tell the difference between Slovakia and Slovenia. They think that it’s just that both guys ‘Vakia’ and ‘Venia’ are ‘slow’. 🙂

    Besides, their disrespectful comments in this blog, although tolerated by some moderators here for unknown to me reasons*, do not motivate to engage in any kind of serious discussion with them.

    Perhaps the only benefit I see from your discussions is that others can read what you write. 🙂

  83. 83
    Dionisio says:

    #98 addendum

    gpuccio

    Your original statement, that has caused so much ‘itching’ to some interlocutors, was written in post #5. It’s really taken too long for some interlocutors to understand it. Oh, well. Things happen. 🙂

  84. 84
    Joe says:

    hrun is confused and cannot follow along. I never said that all genetically engineered splicing’s result in no proteins forming. Never. Not only that hrun cannot present any evidence that amino acid sequence determines shape and function.

    If a gene coding for a protein that does NOT require a chaperone or chaperones to fold then it should do OK in another host. Get one that requires a chaperone or chaperones and it won’t do anything in a foreign host.

  85. 85
    Dionisio says:

    #101 Aurelio Smith

    Vamos, tranquilo amigo, no os preocupéis tanto. Éso ha sido solamente una broma. No os lo toméis tan serio. 🙂

    Not sure whether Dionisio is making a racist slur against people of Spanish ethnicity or is ironically implying that I am racist against people of Spanish ethnicity. Either way it’s pretty despicable.

    I can understand your reaction. But to those who have read my previous comments in this blog, where I have stated on several occasions that I’m Hispanic and my first language is Spanish, my question, immediately followed by a 🙂 was obviously a joke.

    I may be overly sensitive. My mother’s family were Spanish – hence Aurelio.

    Well, I’m much more Hispanic than you are. Born Hispanic, from Hispanic parents, grandparents, etc. Perhaps much earlier in my genealogy tree there were other ethnicities too, because we know that some Mediterranean regions of Spain were occupied by various Middle East or North Africa ethnicities at some points in history, but I have no records of that.

    Now you see that no offense was intended whatsoever. It would have been like attacking my own ethnic roots. But most importantly, I strongly believe that all humans, regardless of ethnicity, cultural background, nationality, social position, anything, share the same dignity that comes from being created by the same Maker, according to the purpose of His will, for His glory. I’m not better than anybody else. However, based on what I know about myself, I’m worse than most people I know. As the apostle Paul said, I’m the chief of sinners. The good news is that God loves us (including you and me). He has graciously offered the Way to reconcile us with Him forever. Hallelujah!

    Espero leer tus próximos comentarios. Anímate y escribe más. Ésta es una vía, quizás un poco más amistosa y relajada, para intercambiar información y opiniones sobre interesantes temas científicos de actualidad.

    Os deseo un buen fin de semana.
    Os saludo cordialmente.

  86. 86
    Dionisio says:

    The structure and function of the eukaryotic ribosome.

    doi: 10.1101/cshperspect.a011536.

    Structures of the bacterial ribosome have provided a framework for understanding universal mechanisms of protein synthesis.

    However, the eukaryotic ribosome is much larger than it is in bacteria, and its activity is fundamentally different in many key ways.

    Recent cryo-electron microscopy reconstructions and X-ray crystal structures of eukaryotic ribosomes and ribosomal subunits now provide an unprecedented opportunity to explore mechanisms of eukaryotic translation and its regulation in atomic detail.

    This review describes the X-ray crystal structures of the Tetrahymena thermophila 40S and 60S subunits and the Saccharomyces cerevisiae 80S ribosome, as well as cryo-electron microscopy reconstructions of translating yeast and plant 80S ribosomes.

    Mechanistic questions about translation in eukaryotes that will require additional structural insights to be resolved are also presented.

    http://www.ncbi.nlm.nih.gov/pubmed/22550233

  87. 87
    hrun0815 says:

    I’m Hispanic and my first language is Spanish, my question, immediately followed by a 🙂 was obviously a joke.

    Ah, yes. Because being part of a group gives license to insult the remainder of the group?

    I understand that you were attempting to make a joke. You failed.

  88. 88
    Dionisio says:

    Structural basis for diversity in the SAM clan of riboswitches.

    doi: 10.1073/pnas.1312918111

    In bacteria, sulfur metabolism is regulated in part by seven known families of riboswitches that bind S-adenosyl-l-methionine (SAM).

    Direct binding of SAM to these mRNA regulatory elements governs a downstream secondary structural switch that communicates with the transcriptional and/or translational expression machinery.

    The most widely distributed SAM-binding riboswitches belong to the SAM clan, comprising three families that share a common SAM-binding core but differ radically in their peripheral architecture.

    Although the structure of the SAM-I member of this clan has been extensively studied, how the alternative peripheral architecture of the other families supports the common SAM-binding core remains unknown.

    http://www.ncbi.nlm.nih.gov/pubmed/24753586

  89. 89
    Dionisio says:

    hrun0815

    Ty umnitsa, prosto molodets!

    🙂 🙂 🙂

  90. 90
    Dionisio says:

    RNA cytidine acetyltransferase of small-subunit ribosomal RNA

    doi: 10.1371/journal.pone.0112156.

    The eukaryotic small-subunit (SSU) ribosomal RNA (rRNA) has two evolutionarily conserved acetylcytidines.

    However, the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified.

    http://www.ncbi.nlm.nih.gov/pubmed/25402480

  91. 91
    Dionisio says:

    A single acetylation of 18 S rRNA is essential for biogenesis of the small ribosomal subunit…

    doi: 10.1074/jbc.M114.593996

    Biogenesis of eukaryotic ribosome is a complex event involving a number of non-ribosomal factors.

    http://www.ncbi.nlm.nih.gov/pubmed/25086048

  92. 92
    AVS says:

    Hey Dio, just a quick question, if you could answer it concisely as possible that would be great.

    What do you think you are accomplishing by copying and pasting the abstracts of all these papers?

  93. 93
    AVS says:

    Or maybe just explain why you highlight things like “the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified.”

  94. 94
    Dionisio says:

    AVS

    Ty umnitsa, prosto molodets!

    🙂

  95. 95
    Dionisio says:

    Aurelio Smith

    Ty umnitsa, prosto molodets!

    🙂

  96. 96
    Dionisio says:

    Movie of the eukaryotic 40S and 60S ribosomal subunits in complex with initiation factors eIF1 and eIF6, respectively.

    The movie visualizes the increased complexity of the eukaryotic ribosome, compared to bacterial and archaeal ribosomes.

    The ribosomal rRNA conserved across all kingdoms is depicted in grey and universally conserved proteins are depicted in light blue.

    Protein and rRNA segments shared between eukaryotes and archaea, but not bacteria are depicted in orange, and segments exclusive to eukaryotes are depicted in red.

    http://www.mol.biol.ethz.ch/gr.....p/Ribosome

  97. 97
    Dionisio says:

    Aurelio Smith

    Since you took it so seriously, then why didn’t you answer the question that triggered your personal attacks the way it should have been answered?

    Didn’t you know the answer?
    Weren’t you sure how to answer it?

    The only correct answer to that question is:

    Yes, of course it can be. The reliability of a document has nothing to do with the ethnicity or cultural background of the authors. That’s a fact attested by many examples in history.

    That should be clear to anyone. But apparently it was not to you when you read the question. Is it now?

    Then, after answering it correctly, thus presenting your strong position on the subject, you could have asked any other question you would have deemed pertinent in order to clarify the subject.

    But that’s not what you did. Why?

    What happened to you?

    Think about it.

  98. 98
    Dionisio says:

    AVS,

    Why do you care so much about what I post or how I do it?

    You’re not the moderator of the thread, nor the administrator of the site.

    If you don’t like it, or it bothers you, you may ignore my posts completely. You don’t have to read them.

    BTW, your derogatory comments are completely worthless. But at times I take the fact that my posts bother you as a tremendous compliment. 🙂

  99. 99
    AVS says:

    Oh Dio.
    Don’t worry, your posts don’t bother me in the least, in fact I find them quite humorous. Some of the papers even sound interesting and I skim through them, so thank you for that!

    I am merely trying to help you out because I fear you have a bit of a misunderstanding as to what you think you are doing.

    Why do you highlight certain statements such as “the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified?”
    It’s a pretty simple question I think, but I’ll understand if you don’t want to answer.

  100. 100
    Dionisio says:

    AVS,

    Why do you highlight certain statements such as “the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified?”

    Ok, that’s a valid question.

    I try and highlight some of the issues that are not explained in the given paper, but may be described in other papers or might be explained in future papers soon.

    This is kind of like a reminder, so that I keep an eye on the given subjects, in order to detect any information that may pop up in another paper and shed more light on some of the issues that currently are poorly described.

    FYI – I’m using Mind Meister + Zotero + various interconnected WordPress web logs to organize (online) the information that I’m gathering, so that I can share it with others (privately) and review it again later, with the help of a few friends who are biologists and a friend who is a scientist working on AI issues.

    For each specific mechanism, seen from an information-processing perspective, I try to see some of the outstanding questions and connect the related ‘dots’ when possible, using newer information that keeps coming in. It’s like trying to complete a puzzle, where the new research papers provide the missing pieces, so everyday the puzzle is getting more complete, but then newer, more detailed puzzles may open up during the process.

    The references I share here are part of the references I’m gathering separately with the online tools I mentioned above. I can’t understand many things, actually I understand very little of what I read, but I try to see if the gathering method and tools work well with this ‘puzzle pieces’ finding approach. It’s like working on an extended ‘proof of concept’ task.

    In order to make things a little easier for me, I’ve narrowed down the area I’m more interested in now, which is related to the mechanisms for the asymmetric mitosis affecting the cell fate specification and determination. But other areas are very interesting too. In Biology many things are interesting, but I can only look into a very small fraction of the whole picture without loosing my sanity. 🙂

    These are fascinating times to watch the advance of scientific research. I’m sure we all agree on this.
    Every new discovery sheds more light on very interesting biological systems.
    Working on this is not easy for me, because I’m new in this area and know very little, even after taking online biology 101 classes offered by some universities free of charge.
    A parallel project includes interactive 4D animation software development, which I’ve started on C++/C# .NET with some XAML, using the MSVS IDE, but lately considering to do it in Xamarin and Azure environments.
    All this is difficult, although the most difficult part is understanding enough biology just to find the missing pieces of the puzzle and test the information-gathering method.
    Both, the studying and the software development issues consume a substantial part of my limited time. Some of my colleagues would have done all this much faster than I can, but they just don’t feel the same attraction to biology, hence they don’t want to work on this.

    Did I answer your question properly?

    Please, let me know. Thank you.

    PS. Did you understand what I wrote to you @112? Perhaps you will like it. It’s something my classmates sometimes said to each other at the university. I don’t recall anyone saying that to me, though. The original version is in the Cyrillic alphabet, but in this blog it’s easier for me to write the phonetic version using the English alphabet.

  101. 101
    hrun0815 says:

    I try and highlight some of the issues that are not explained in the given paper, but may be described in other papers or might be explained in future papers soon.

    This is kind of like a reminder, so that I keep an eye on the given subjects, in order to detect any information that may pop up in another paper and shed more light on some of the issues that currently are poorly described.

    […]

    I can’t understand many things, actually I understand very little of what I read, but I try to see if the gathering method and tools work well with this ‘puzzle pieces’ finding approach. It’s like working on an extended ‘proof of concept’ task.

    Have you considered that rather than putting all this work into this puzzle pieces approach it might be more useful to learn how to properly read and understand maybe a single paper you ‘collect’.

    It seems relatively obvious that without actually understanding the papers it is going to be difficult for you to evaluate any of them. And it is not totally clear how you think you can ‘detect any information that may pop up in another paper and shed more light on some of the issues that currently are poorly described’ if according to your own admission you ‘understand very little of what [you] read’.

  102. 102
    AVS says:

    That’s what I was afraid of Dio.
    The majority of the things you highlight “that are not explained in the given paper,” are in fact explained in the paper.
    I’m surprised none of your “biologist” friends have pointed this out to you yet actually.
    You see, what happens is in most cellular biology papers a question or unsolved problem is highlighted in the abstract, and then the paper goes onto explain the answer or at least part of it.

    Let’s take that paper I mentioned: “the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified,” it waht you highlighted.

    The paper then goes on to specifically identify the acetyltransferase and the acetylation site. This is why part of the paper’s title is “identification of acetylation sites and the responsible acetyltransferase in fission yeast, Schizosaccharomyces pombe”

    This is most likely due to the fact that you don’t actually read the majority of the paper and that you certainly don’t understand what you do read.

    I don’t know what to say Dio, but it’s not looking good for you. It sounds like you are just compiling the most useless list of publications known to man.

  103. 103
    Dionisio says:

    AVS,

    They identified Nat10 as the enzyme responsible for the cytidine acetylation, which seems like the explicit objective of that paper, according to the title and the abstract, but I did not find where they explain how Nat10 got in the picture, at the right time, in the right place, in the right amount required for the cytidine acetylation.

    There are several conditional statements that should be clarified for a software development project, that perhaps are not required for the paper to be understood by other biologists.

    Apparently there is assumed knowledge that is not explicitly available to non-biologists.

    Perhaps that’s explained in the rest of the paper, or maybe not, that’s why I highlight the statement so that I have a reminder to keep looking for those pieces that may not be explained in the paper, but somewhere else, because maybe they are obvious things assumed by the biology researchers, but unknown to the system analysts working on the programming specs.

    When developing software, no detail can be left out of the picture. Biologists know many things that they assume known by their colleagues who will read their papers, but software analysts, engineers, developers, don’t know many things about biology, but still have to develop a software that deals with those concepts they don’t know.

    Perhaps that’s one of the reasons the concept of interdisciplinary teamwork has reached some level of acceptance in academic and research circles these days.

    Ideally, the software should be designed, developed, tested, implemented, supported, by the same biologists. But they are busy working on difficult and time consuming research, hence don’t have any time left for other endeavors.

    Have you ever worked on engineering software development projects? Are you familiar with the process that precedes the actual programming? The creation of the tech documentation to write the programming specs?

    Again, no details should be left out. Not one. Before the programmers get to work coding the myriad of instructions that make the system, the tech specs must be precisely defined, no ambiguities are allowed, no ‘maybes’ or ‘perhaps’ or ‘suppositions’.

    Interactive animation software development deals with the fact that the user can modify the conditions continuously, in order to test different scenarios and choreographies for every given story within a project. Hence the tech specs must consider all the possible variants, either in implicit generic terms, or in explicit lists of cases. All the objects involved in every choreography must be associated with a detailed description of the conditions that cause the object to appear on the scene, what it does, how it does it, etc.

    Are we starting to understand each other better now?

    I appreciate you have decided to engage in a serious discussion with me on this subject. Maybe you could provide the details I’m looking for, thus saving me a substantial amount of time that I could use somewhere else.

    🙂

  104. 104
    Dionisio says:

    #119 hrun0815

    Obviously you grossly misunderstood what I wrote, hence you’ve jumped into wrong conclusions that took you farther away from the main subject.

    At least AVS asked some questions before arriving at wrong conclusions, but you didn’t even try to clarify the situation before giving your opinion.

    I suggest you read post #121 or simply refrain from writing ridiculously disoriented opinions on this subject.

    Enjoy the weekend.

    🙂

  105. 105
    hrun0815 says:

    Obviously you grossly misunderstood what I wrote, hence you’ve jumped into wrong conclusions that took you farther away from the main subject.

    Strange. Even after reading your post #121 it seems that I perfectly well understood what you wrote.

    At least AVS asked some questions before arriving at wrong conclusions, but you didn’t even try to clarify the situation before giving your opinion.

    It turns out that I am actually able to read any of the questions and answers that get posted here. It is therefor irrelevant who actually asks these questions of you.

    I suggest you read post #121 or simply refrain from writing ridiculously disoriented opinions on this subject.

    It is a ‘ridiculously disoriented’ opinion that rather than collecting papers you actually learn to understand them first? Or are you claiming that you actually understand the papers perfectly well and your statement “actually I understand very little of what I read” refers to something completely different? Or maybe when you write “Apparently there is assumed knowledge that is not explicitly available to non-biologists.” this does not mean that you actually lack this knowledge?

    Ideally, the software should be designed, developed, tested, implemented, supported, by the same biologists. But they are busy working on difficult and time consuming research, hence don’t have any time left for other endeavors.

    At least here I agree with you. That’s why in all cases I know of such software is indeed always designed, developed, tested, and implemented by biologists or in close collaboration with biologists.

    You should take your own advice to heart rather than ignoring it. Maybe, just maybe, if it turns out that you can’t find biologists to collaborate on your project you either need to put a bit more effort into finding such collaborators or you should examine if maybe this project is not of any worth to biologists (hence their reluctance to collaborate with you on this).

    Anyway, just some thoughts. Feel free to write them off as ‘ridiculously disoriented opinions’. It’s your time and you can spend it on whatever floats your boat.

  106. 106
    Dionisio says:

    #123 hrun0815

    Why does it bother you that I collect the papers without understanding them?

    Does that violate any rule in this blog or somewhere else?

    BTW, this is supposed to be an educational software. Not to please biologists.

    Would you like to collaborate? How much would you charge per hour of consultation? Can you answer the questions I asked @121 about the enzyme Nat10? Why does it appear on the scene, when, how, how many?

    The researchers I’ve contacted so far work on diabetes, allergy, stem cells, protein folding, respectively. They have said my approach seems correct, as far as they could understand it. They can’t work on this project because they don’t have much time left after family and work.

  107. 107
    hrun0815 says:

    Why does it bother you that I collect the papers without understanding them?

    Does that violate any rule in this blog or somewhere else?

    Nope. Not at all. That’s why I wrote:

    It’s your time and you can spend it on whatever floats your boat.

    As hard as it might be for you to believe, this is actually just advice. And considering your stated desires probably relatively good advice, too.

    Think about it some more:

    That’s why in all cases I know of such software is indeed always designed, developed, tested, and implemented by biologists or in close collaboration with biologists.

    You should take your own advice to heart rather than ignoring it. Maybe, just maybe, if it turns out that you can’t find biologists to collaborate on your project you either need to put a bit more effort into finding such collaborators or you should examine if maybe this project is not of any worth to biologists (hence their reluctance to collaborate with you on this).

  108. 108
    Dionisio says:

    #125 hrun0815

    Would you like to collaborate?
    How much would you charge per hour of consultation?

    Can you answer the questions I implicitly asked @121 about the enzyme Nat10? Why does it appear on the scene (i.e. what events trigger it), when, how does that happen, how many of them, what determines the right amount (if there is such)? Are these questions answered in the paper, as AVS seemed to claim?

    The project is moving well. Perhaps it’s a little behind schedule, but that’s fine. The main goal is achievable within a reasonable timeframe.

  109. 109
    AVS says:

    The explicit objective of the paper was to present information on “identification of acetylation sites and the responsible acetyltransferase in fission yeast, Schizosaccharomyces pombe.” And they did both.

    I repeat, the question you highlighted because you thought it was “not explained in the given paper,” was explained in the given paper. I didn’t arrive at any wrong conclusions, don’t worry.

    Were just trying to help you out!

  110. 110
    hrun0815 says:

    Would you like to collaborate?
    How much would you charge per hour of consultation?

    How could I decide if I want to collaborate without knowing the first thing about your project other than that it is some sort of software project tied to biology? And before you inquire about my rate for consultation wouldn’t you first want to establish if my expertise is actually relevant to what you are trying to achieve?

    Can you answer the questions I implicitly asked @121 about the enzyme Nat10? Why does it appear on the scene (i.e. what events trigger it), when, how does that happen, how many of them, what determines the right amount (if there is such)? Are these questions answered in the paper, as AVS seemed to claim?

    Again, how do you think did I misinterpret what you were writing before? The last question you ask only leaves two possibilities: Either you do not actually have access to the whole paper and are trying to make sense of it from the publicly available abstract alone or you are unable to understand the paper.

    In either case, my two suggestions to you are:

    1) Figure out how to get access and understand the complete papers rather than searching through abstracts alone.
    2) Figure out if biologists are interested in your project and find somebody to work with.

  111. 111
    Dionisio says:

    AVS,

    The paper resolved the main issue in the title, but from a software development point of view, they left unanswered questions, perhaps because it was known to other biologists, but not to me. Hence I highlight that text as a reminder to indicate that the given explanation may not contain explicitly all the details required for the 4D simulation software.

    Apparently you did not understand well what I wrote in my previous posts here. You may want to read it all again, carefully.

    Can you tell me where in the given paper they answer the questions I implicitly asked @121 about the enzyme Nat10? Why does it appear on the scene (i.e. what events trigger it), when, how does that happen, how many of them, what determines the right amount (if there is such)?

    Are those questions answered explicitly in the paper, but I did not understand it? Are they assumed knowledge the biologists have, but I have to still look for a text where it is explained explicitly? Can you respond these questions, and indicate what document you find that information in? Thank you.

  112. 112
    Dionisio says:

    #128 hrun0815

    You have not answered the questions about Nat10, which I asked you in post #126 and you posted @128.

    Can you tell me where in the given paper they answer the questions I implicitly asked @121 about the enzyme Nat10? Why does it appear on the scene (i.e. what events trigger it), when, how does that happen, how many of them, what determines the right amount (if there is such)?

    Are those questions answered explicitly in the paper, but I did not understand it? Are they assumed knowledge the biologists have, but I have to still look for a text where it is explained explicitly? Can you respond these questions, and indicate what document you find that information in? Thank you.

    No, I don’t have access to most paywalled papers, that’s why I highlight text in the abstract, as a reminder to keep looking for the missing details. Later I may ask my friends, who do have access to those papers, to see whether the information I’m looking for is in the given papers or not. Or I keep looking for that information somewhere else online. That’s why the search is so extensive. The references I share here are part of the ones I gather, in a more organized manner, within Zotero, which detects duplicate references, and has hierarchical trees of folders and subfolders, tagging, and other cool features that facilitate the reviewing of the information.

    Now, please, go back to the above highlighted text and answer those questions. Or simply tell me you don’t know the answer either. Thank you.

  113. 113
    Dionisio says:

    AVS

    Please, read post #130 and see if you can help hrun0815 to answer my questions about the given paper, which you chose to discuss in this thread. Thank you.

    Since you two chose to discuss this with me here, let’s take it to a valid conclusion.

  114. 114
    Dionisio says:

    AVS

    As you well know, N-acetyltransferase 10 is an enzyme that in humans is encoded by the NAT10 gene. I just read it online. There are many online references to this enzyme. There’s some reading there, but it was not in my plan to read about this now. However, since you brought it up,…

    But when is Nat10 produced for the case of the discussed paper? what triggers that gene expression in relation to the discussed paper? what amount? or is it produced constantly? or is it produced for other processes and just happen to be available for the discussed process too?

    Perhaps those are easy questions for you, but not for me. Remember that I’m not a biologist, just a software developer, with engineering background. That’s why I highlight text to remind myself that more search is required for my project, if the given issue ends up in the final example for the software testing and user documentation.

    Can you answer the questions I asked you in 129 and repeated for hrun0815 in 130? Well, they have been implicitly asked since post 121.

  115. 115
    Dionisio says:

    AVS and hrun0815

    Again, I appreciate that you have decided to discuss this ‘highlighting’ style issue with me here.

    Perhaps together we’ll be able to clarify a few things, four our mutual benefit.

    Please, respond the questions about Nat10, so that we can move on and I can ask you other questions related to other issues also left unanswered in the given paper.

  116. 116
    Dionisio says:

    NAT10, a nucleolar protein, localizes to the midbody and regulates cytokinesis and acetylation of microtubules.

    DOI: 10.1016/j.yexcr.2009.03.007

    http://www.researchgate.net/pu.....crotubules

  117. 117
    Dionisio says:

    Chemical Inhibition of NAT10 Corrects Defects of Laminopathic Cells.

    DOI: 10.1126/science.1252651

    http://www.researchgate.net/pu.....thic_Cells

  118. 118
    Dionisio says:

    The Complexity of Human Ribosome Biogenesis Revealed by Systematic Nucleolar Screening of Pre-rRNA Processing Factors

    doi:10.1016/j.molcel.2013.08.011

    Mature ribosomal RNAs (rRNAs) are produced from polycistronic precursors following complex processing.

    …human cells adopt unique strategies and recruit distinct trans-acting factors to carry out essential processing steps, posing fundamental implications for understanding ribosomopathies at the molecular level…

    http://www.sciencedirect.com/s.....6513005844

  119. 119
    Dionisio says:

    AVS and hrun0815

    See post #136 for another example of my highlighting style that has so bothered you.

    Note that sometimes I highlight text that might require additional search in other to complete the puzzle using the information available in the same paper or in other papers.

    When you see a verb highlighted, it may indicate that I may have to look for the definition of that given action within the given context, and a detailed description of the given action.

    Are we starting to understand each other now?

    Can you show me that you have understood what I meant in my previous posts that caused so much discussion here?

    Are we seeing light at the end of the tunnel yet?

    Bottom line, were my questions about Nat10 answered within the paper AVS chose to discuss, or outside that paper?

    If you answer the preceding question, we can move on.

    Thanks.

  120. 120
    Dionisio says:

    AVS,

    Is Nat10 a systemic enzyme that’s available all the time in the nucleus? How is the expression of the gene NAT10 regulated? Those are known facts to biologists, but not to me. Do you see the difference? That’s why I highlight things you may not need to because you already know all that.

  121. 121
    hrun0815 says:

    Dionisio, I think you still don’t understand the tenor of my comments or advice.

    IF you want to base any kind of useful work on the published work then you have to make sure you actually are able to access all the relevant published work AND you have to make sure that you can somehow understand the relevant published work. It looks to me that in this case neither is the case.

    In both respects your nearest local university is probably your best bet. Go to the library and see if the relevant journals are available. If not, you can get them for a small fee (which at some universities is waved) through inter-library loan programs. Alternatively, you can actually write to the corresponding author on the paper to ask for a reprint (these days a pdf of the complete paper).

    As for understanding the papers and the missing biological assumptions there is no substitute for a trained biologist in the relevant field. Either you learn it yourself which will be extremely time consuming or you find an actual collaborator. A collaborator in this case is somebody who is vested in your project and has their own motivation for the project to succeed. In your case I presume that there is a very limited budget for the project, so I would not recommend subcontracting this (paying a biologist a fee for their work). Subcontracts are notoriously expensive (at least in the US) and you generally get much better work from a truly interested biologist. For starters, a subcontractor may not actually advise you properly on the importance of the work (they are mainly interested in keeping a project going), while a collaborating biologist will of course tell you if the project is not worth their (and your) time.

    Finding some guys on the internet to answer a few questions about one paper (out of many dozens or even hundreds) you are interested in is no substitute. For starters, how do you know you can even trust any of the info you’d be getting from me or AVS? Would we attach our name to the work to take responsibility for it?

    Anyway, my guess is that you will disregard this advice, and, again, this is of course your prerogative. It is your time, your project, and you are solely responsible for its success or failure.

    Cheers… hrun

    PS: And here is the answer to your specific question. My guess is that you will use this answer to justify discarding my more general advice:

    I do not know the answers to your questions. I have no interest in reading the paper. It’s not in a field I am interested in and I already have way more papers to read than I can reasonably get through. Also, I have little interest in attempting to exactly parse your questions either or hash out in what detail the answers are known or why the answers are even relevant to whatever project you are working on.

    Again, that’s why I would strongly urge you to collaborate with an interested biologist who has good motivation in walking you through your open questions.

  122. 122
    DNA_Jock says:

    Dionisio,

    when is Nat10 produced for the case of the discussed paper? what triggers that gene expression in relation to the discussed paper? what amount? or is it produced constantly? or is it produced for other processes and just happen to be available for the discussed process too?

    I have an offer for you. I will provide the answers (including references) to these questions for free, if you first provide the URL for the text that you pasted into comment 107.

    If you find this offer unappealing, I’ll understand.

  123. 123
    Dionisio says:

    #139 hrun0815

    I do not know the answers to your questions. I have no interest in reading the paper. It’s not in a field I am interested in and I already have way more papers to read than I can reasonably get through. Also, I have little interest in attempting to exactly parse your questions either or hash out in what detail the answers are known or why the answers are even relevant to whatever project you are working on.

    That’s fine. But then why did you get involved in this discussion after all? Why did you volunteered your unsolicited opinion on the discussed subject? At least AVS pointed to a specific issue he misunderstood (and apparently still doesn’t understand well) in my posts, but you jumped into wrong conclusions and gave pontificating opinions.

    In your case, someone else would rather refrain from getting involved in the discussion. If one sees a post that is not understood well, but it’s related to a subject that one doesn’t know and/or doesn’t care much about, one simply ignore it. That happens to me all the time in this blog and everywhere around.

    Your unsolicited opinion could have indicated that you know the discussed subject and are interested in it. Now, when the heat of my direct questions cornered you against the wall, you felt forced to confess (reveal, admit) your lack of interest in this discussion and your poor knowledge of the subject details.

    Next time just ignore my posts, skip them. No one can force you to get involved in any discussion here. Basically, don’t provoke others. Unless you change your mind and decide to learn about biology seen from a software development perspective, where all the conditions that may affect the programming decisions, must be precisely described in all the necessary details, in the tech specs the programmers follow in order to code the logic of the developed system. There’s more to this than what I just wrote, but in a nutshell that’s basically it. Now you know for next time.

  124. 124
    hrun0815 says:

    Dionisio writes at 9:15am:

    That’s fine. But then why did you get involved in this discussion after all?

    Hrun0815 wrote at 8:15am:

    My guess is that you will use this answer to justify discarding my more general advice […]

    and

    […] this is of course your prerogative. It is your time, your project, and you are solely responsible for its success or failure.

    What a surprise.

    Your unsolicited opinion could have indicated that you know the discussed subject and are interested in it. Now, when the heat of my direct questions cornered you against the wall, you felt forced to confess (reveal, admit) your lack of interest in this discussion and your poor knowledge of the subject details.

    Maybe it could be that rather than knowing something about the one paper I know something about software engineering and development in biology? In fact, if you lack back at my recent posts you will find that this is the topic I was referring to?

    In your case, someone else would rather refrain from getting involved in the discussion.

    Or not? Who cares? Just like your time is yours to spend how you like, mine is mine alone (well maybe my family has a claim on it as well).

    Unless you change your mind and decide to learn about biology seen from a software development perspective, where all the conditions that may affect the programming decisions, must be precisely described in all the necessary details, in the tech specs the programmers follow in order to code the logic of the developed system. There’s more to this than what I just wrote, but in a nutshell that’s basically it. Now you know for next time.

    Just like you had NO IDEA about my knowledge of the specific paper in question you also have NO IDEA about my knowledge regarding biology as seen from a software development perspective.

    The beauty of my comments is that you can evaluate without knowing anything about the author if they are useful or not. From your answer here I can probably readily deduce your decision on this. Again… your time and your prerogative.

    Here is yet another bit of ‘unsolicited’ and ‘pontificating’ opinion: If you do not believe me or can not see the logic in what I am saying I would suggest you look for the nearest Systems Biology Department or contact some people there by email (a solid Bioinformatics Department would also do the trick). Find a few of the many software engineers there and have a brief conversation about my advice here. You’ll likely be surprised. 🙂

  125. 125
    hrun0815 says:

    DNA_Jock:

    I have an offer for you. I will provide the answers (including references) to these questions for free, if you first provide the URL for the text that you pasted into comment 107.

    I don’t understand. I believe he did provide the URL. The quote is taken directly from PubMed (or PLOS or PMC).

    Did you mean a different post?

  126. 126
    DNA_Jock says:

    hrun,
    I would like Dionisio to confirm the specific URL that he used to copy the text he used in 107. If it was the pubmed link he provided in that post, then answering will be really easy…

  127. 127
    Dionisio says:

    #140 DNA_Jock

    I have an offer for you. I will provide the answers (including references) to these questions for free, if you first provide the URL for the text that you pasted into comment 107.
    If you find this offer unappealing, I’ll understand.

    Did you read my posts in this thread, after AVS initiated this latest discussion by posting his comments and/or questions @ 109 & 110?

    If you did, then it seems like you did not understand my point.

    Can you tell me briefly (in a nutshell), what you understood is the main idea expressed in my posts?

    Remember that understanding someone else’s message does not imply agreeing with it at all. But communication can’t be efficient and discussions can’t be productive, unless both sides are willing to understand each other very well, though still they may disagree.

    The bottom line of my posts was to answer AVS’ initial questions on why I highlight certain text in some of my posts. The highlighting is a way of reminding myself about possible areas of additional search for details that may be in the given paywalled paper or in other papers or textbooks.

    Note that there are verbs highlighted in some posts, keywords in others, or entire expressions in some of the posts.

    Within the web logs linked from Zotero and Mind Meister, the highlighting is more dynamic, keeps changing as information is found and newer questions pop up, even causing new deeper layers of search to appear either as subfolders in an existing branch within Zotero or a separate link in Mind Meister or another post in the linked web logs.

    This is a new and very challenging experience for me, but I’m enjoying it very much. It’s kind of fun too. As I said, my more experienced and sharper colleagues could have done this project much faster, but they just don’t care much about the biology part. Simply don’t feel the attraction to it. Hence they did not embark on this thrilling journey along with me. I fully understand their position. They prefer complex engineering stuff that are better documented and where one can talk anytime to the expert engineers to get all the required explanations about their way of doing things, in order to reflect their ideas in the tech specs for the programmers.

    To me this is a wonderful learning experience too.

    The papers I share here in this site are part of the whole database of references gathered in the online tools mentioned above.

    In the specific case AVS pointed to, there are many details that are unknown to me, but I don’t need them now, so I mark up the text as a reminder for future search, if it comes to that. I may not get back to it at all, but someone else could follow up.

    Later, after reviewing the references, stored in Zotero (tagged, sorted, hierarchically organized in subfolders) and with the associations between different Zotero branches graphically visualized in Mind Meister, or referenced in a set of restricted WordPress web logs, then I could decide to search a particular detail further, to dig deeper, or simply leave that particular ‘branch’ of info alone (shelved/on the back burner) and move on with other details, according to the progress of the system implementation schedule and priorities.

    The highlighted text in the web log posts may be associated with different tags in the Zotero information or with links in the Mind Meister interconnected maps.

    Perhaps others out there have better systems to reference all that information in easier ways to access it. This approach I’m taking is not mine originally, but was suggested by colleagues and friends. They recommended the online tools and the general approach. They are quite flexible. The online accounts may be setup and owned by someone who shares them with me and allows me to modify the information or add new one. Really cool. I recommend it too. But perhaps most folks in this site have used these or other similar tools for their research projects.

    Anyway, the project seems to be moving ahead well, though a little behind schedule (what else is new?).

    Have a good day.

  128. 128
    Dionisio says:

    Human NAT10 Is an ATP-dependent RNA Acetyltransferase Responsible for N4-Acetylcytidine Formation in 18 S Ribosomal RNA (rRNA).

    doi: 10.1074/jbc.C114.602698

    Human N-acetyltransferase 10 (NAT10) is known to be a lysine acetyltransferase that targets microtubules and histones and plays an important role in cell division.

    http://www.ncbi.nlm.nih.gov/pubmed/25411247

  129. 129
    DNA_Jock says:

    Dionisio,

    when is Nat10 produced for the case of the discussed paper? what triggers that gene expression in relation to the discussed paper? what amount? or is it produced constantly? or is it produced for other processes and just happen to be available for the discussed process too?

    I have an offer for you. I will provide the answers (including references) to these questions for free, if you first provide the URL for the text that you pasted into comment 107.
    If you find this offer unappealing, I’ll understand.

    So you do find this offer unappealing, as I expected. I understand. Perfectly.
    😉

    P.S. Your 145 reminds me somewhat of Gary Gaulin…

  130. 130
    hrun0815 says:

    So you do find this offer unappealing, as I expected. I understand. Perfectly.

    Heh. That surprisingly came out exactly as you suspected. However, I must admit, I do not understand. Not perfectly. Not a little bit. Nothing.

    What prevented Dio from just C/P the PubMed link from 107 and then get the answers he was supposedly looking for? And even if he was not actually looking for those answers, why not just C/P and pretend that you are? Why repeat the endless description of his paper collection process?

  131. 131
    Dionisio says:

    [In vivo functions of long non-coding RNAs].

    Advances in genomics and molecular biology have led to discovery of a large group of previous uncharacterized long non-noncoding RNAs (lncRNAs).

    Whether all of these transcripts are functional remains to be elucidated, but emerging evidence indicates that many lncRNAs play roles in multiple biological processes and that dysregulation of lncRNAs is often associated with diseases.

    Of significant interest, recent studies suggest that almost all of the regulatory lncRNAs function through interacting with different biological macromolecules such as DNA, RNA, and protein.

    In this review, we summarize the mechanisms by which lncRNAs regulate gene expression at epigenetic, transcriptional and post-transcriptional levels, and discuss the role of lncRNAs in tumorigenesis and host defense.

    Distinct from small ncRNAs that regulate gene expression mainly through base pairing to target transcripts, most identified lncRNAs function by regulating protein activity or maintaining the integrity of protein complexes.

    As a result, identification and characterization of the lncRNA-protein interactions may be the primary task to decode functional lncRNAs.

    http://www.ncbi.nlm.nih.gov/pubmed/24846963

  132. 132
    Dionisio says:

    Epigenetic coordination of embryonic heart transcription by dynamically regulated long noncoding RNAs

    doi: 10.1073/pnas.1410622111

    The vast majority of mammalian DNA does not encode for proteins but instead is transcribed into noncoding (nc)RNAs having diverse regulatory functions.

    The poorly characterized subclass of long ncRNAs (lncRNAs) can epigenetically regulate protein-coding genes by interacting locally in cis or distally in trans.

    A few reports have implicated specific lncRNAs in cardiac development or failure, but precise details of lncRNAs expressed in hearts and how their expression may be altered during embryonic heart development or by adult heart disease is unknown.

    Analysis of protein-coding mRNAs from the same samples identified 22 concordantly and 11 reciprocally regulated mRNAs within 10 kb of dynamically expressed lncRNAs, and reciprocal relationships of lncRNA and mRNA levels were validated for the Mccc1 and Relb genes using in vitro lncRNA knockdown in C2C12 cells.

    Network analysis suggested a central role for lncRNAs in modulating NF?B- and CREB1-regulated genes during embryonic heart growth and identified multiple mRNAs within these pathways that are also regulated, but independently of lncRNAs.

    http://www.ncbi.nlm.nih.gov/pubmed/25071214

  133. 133
    DNA_Jock says:

    hrun
    What prevented Dio from just C/P the PubMed link from 107 and then get the answers he was supposedly looking for? And even if he was not actually looking for those answers, why not just C/P and pretend that you are? Why repeat the endless description of his paper collection process?

    What indeed?

    But rather than answer my simple question (and obtain the information he claims to seek), we get Brave Sir Robin and the Green Midget Cafe (x12).

    Cracks me up every time.

  134. 134
    Dionisio says:

    Proteome Software Products
    http://www.proteomesoftware.com/products/

    Proteomics & Bioinformatics
    http://proteomicsconference.com/

    HUPO 2014 last October in Madrid
    http://www.hupo2014.com/

    HUPO 2015 in Vancouver
    http://www.hupo.org/

    Proteome Science &
    Computational Biology
    http://www.hoajonline.com/Jour.....ional.html

    The Human Proteome (D7)
    In Stockholm this April
    http://www.keystonesymposia.org/15D7

  135. 135
    Dionisio says:

    Functional annotation of proteome encoded by human chromosome 22.

    doi: 10.1021/pr401169d

    As part of the chromosome-centric human proteome project (C-HPP) initiative, we report our progress on the annotation of chromosome 22.

    Chromosome 22, spanning 51 million base pairs, was the first chromosome to be sequenced.

    Gene dosage alterations on this chromosome have been shown to be associated with a number of congenital anomalies.

    In addition, several rare but aggressive tumors have been associated with this chromosome.

    A number of important gene families including immunoglobulin lambda locus, Crystallin beta family, and APOBEC gene family are located on this chromosome.

    On the basis of proteomic profiling of 30 histologically normal tissues and cells using high-resolution mass spectrometry, we show protein evidence of 367 genes on chromosome 22.

    Importantly, this includes 47 proteins, which are currently annotated as “missing” proteins.

    We also confirmed the translation start sites of 120 chromosome 22-encoded proteins.

    Employing a comprehensive proteogenomics analysis pipeline, we provide evidence of novel coding regions on this chromosome which include upstream ORFs and novel exons in addition to correcting existing gene structures.

    We describe tissue-wise expression of the proteins and the distribution of gene families on this chromosome.

    These data have been deposited to ProteomeXchange with the identifier PXD000561.

    http://www.ncbi.nlm.nih.gov/pubmed/24669763

  136. 136
    Dionisio says:

    In silico prediction of structure and functions for some proteins of male-specific region of the human Y chromosome.

    doi: 10.1007/s12539-013-0178-5

    […]

    The results of these structure-functional annotations provide a comprehensive view of the proteins encoded by MSY, which sheds light on their biological functions and molecular mechanisms.

    […]

    http://www.ncbi.nlm.nih.gov/pubmed/24402818

  137. 137
    Dionisio says:

    Causal signals between codon bias, mRNA structure, and the efficiency of translation and elongation

    doi: 10.15252/msb.20145524.

    Ribosome profiling data report on the distribution of translating ribosomes, at steady-state, with codon-level resolution.

    http://www.ncbi.nlm.nih.gov/pubmed/25538139

  138. 138
    Dionisio says:

    Lysine glutarylation is a protein posttranslational modification regulated by SIRT5.

    doi: 10.1016/j.cmet.2014.03.014.

    We report the identification and characterization of a five-carbon protein posttranslational modification (PTM) called lysine glutarylation (Kglu).

    http://www.ncbi.nlm.nih.gov/pubmed/24703693

  139. 139
    Dionisio says:

    Alternate deacylating specificities of the archaeal sirtuins Sir2Af1 and Sir2Af2

    doi: 10.1002/pro.2546.

    Sirtuins were originally shown to regulate a wide array of biological processes such as transcription, genomic stability, and metabolism by catalyzing the NAD(+) -dependent deacetylation of lysine residues.

    Recent proteomic studies have revealed a much wider array of lysine acyl modifications in vivo than was previously known, which has prompted a reevaluation of sirtuin substrate specificity.

    Several sirtuins have now been shown to preferentially remove propionyl, succinyl, and long-chain fatty acyl groups from lysines, which has changed our understanding of sirtuin biology.

    In light of these developments, we revisited the acyl specificity of several well-studied archaeal and bacterial sirtuins.

    We find that the Archaeoglobus fulgidus sirtuins, Sir2Af1 and Sir2Af2, preferentially remove succinyl and myristoyl groups, respectively.

    Crystal structures of Sir2Af1 bound to a succinylated peptide and Sir2Af2 bound to a myristoylated peptide show how the active site of each enzyme accommodates a noncanonical acyl chain.

    As compared to its structure in complex with an acetylated peptide, Sir2Af2 undergoes a conformational change that expands the active site to accommodate the myristoyl group.

    These findings point to both structural and biochemical plasticity in sirtuin active sites and provide further evidence that sirtuins from all three domains of life catalyze noncanonical deacylation.

    http://www.ncbi.nlm.nih.gov/pubmed/25200501

  140. 140
    Dionisio says:

    Post-translational modifications: SUMO size me

    doi:10.1038/nchembio.1674

    The reversible attachment of small ubiquitin-like modifier (SUMO) proteins to the lysine side chains of specific proteins is necessary for genome stability and transcription.

    http://www.nature.com/nchembio......1674.html

  141. 141
    Dionisio says:

    Post-translational modifications are the chemical modifications of proteins subsequent to their biosynthesis.

    The modification of certain amino acid residues may result in changes of the protein conformation and/or its capacity to interact with other proteins or ligands, to be active or inactive in the case of an enzyme, to allow or interfere with gene expression and many other biological functions.

    http://www.biosyn.com/tew/prot.....fragment_=

  142. 142
    Dionisio says:

    Posttranslational modification of Sirt6 activity by peroxynitrite

    doi:10.1016/j.freeradbiomed.2014.11.011

    http://www.sciencedirect.com/s.....4914013744

  143. 143
    DNA_Jock says:

    Hrun0815,

    As Dionisio has gone all Lobster Thermidor, I will explain why I expected him to find my offer unappealing.
    Dionisio’s original post @107

    RNA cytidine acetyltransferase of small-subunit ribosomal RNA
    doi: 10.1371/journal.pone.0112156.
    The eukaryotic small-subunit (SSU) ribosomal RNA (rRNA) has two evolutionarily conserved acetylcytidines.
    However,the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified.
    http://www.ncbi.nlm.nih.gov/pubmed/25402480

    AVS asked him why he highlights particular phrases in his C&P’s.
    He replied @118

    AVS,

    Why do you highlight certain statements such as “the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified?”

    Ok, that’s a valid question.
    I try and highlight some of the issues that are not explained in the given paper, but may be described in other papers or might be explained in future papers soon.
    This is kind of like a reminder, so that I keep an eye on the given subjects, in order to detect any information that may pop up in another paper and shed more light on some of the issues that currently are poorly described.

    Now, I was fairly confident that Dionisio’s source for the text he pasted included the full title of the article, which is
    “RNA cytidine acetyltransferase of small-subunit ribosomal RNA: identification of acetylation sites and the responsible acetyltransferase in fission yeast, Schizosaccharomyces pombe.”

    Thus Dionisio, by revealing the source of his text, would be admitting that he went to the effort of separating the colon from the “RNA” when he carefully deleted the second half of the title
    “: identification of acetylation sites and the responsible acetyltransferase in fission yeast, Schizosaccharomyces pombe.”

    And then bolded this phrase from the abstract

    “the acetylation sites and the acetyltransferase responsible for the acetylation have not been identified.”

    because it was one of the

    “issues that are not explained in the given paper”.

    That’s pretty blatant…

    Now, I cannot know whether Dionisio realized that this specific point was where I was heading, or whether he merely suspected a trap. Given that he is not actually interested in getting his questions answered, merely in posing them for rhetorical effect, I was confident he would find my offer unattractive.
    As AVS noted, Dionisio’s technique is quite transparent. Here’s another fun example:
    Dionisio @105

    Structural basis for diversity in the SAM clan of riboswitches.
    doi: 10.1073/pnas.1312918111
    In bacteria, sulfur metabolism is regulated in part by seven known families of riboswitches that bind S-adenosyl-l-methionine (SAM).
    Direct binding of SAM to these mRNA regulatory elements governs a downstream secondary structural switch that communicates with the transcriptional and/or translational expression machinery.
    The most widely distributed SAM-binding riboswitches belong to the SAM clan, comprising three families that share a common SAM-binding core but differ radically in their peripheral architecture.
    Although the structure of the SAM-I member of this clan has been extensively studied, how the alternative peripheral architecture of the other families supports the common SAM-binding core remains unknown.
    http://www.ncbi.nlm.nih.gov/pubmed/24753586

    Cool, so one of Dio’s “issues that are not explained in the given paper” is “how the alternative peripheral architecture of the other families supports the common SAM-binding core remains unknown”.
    The sentence immediately following the one he bolded reads

    We have therefore solved the X-ray structure of a member of the SAM-I/IV family containing the alternative “PK-2” subdomain shared with the SAM-IV family.

    You couldn’t make this stuff up. Really.

  144. 144
    Dionisio says:

    #161 DNA_Jock

    Can you answer my questions in posts #129-133 and 137-138?

    Remember, don’t leave any potential questions unanswered, at any level of details, because the unanswered questions might come back to you like boomerangs.

    Please, note that if your answer includes references to papers, please, quote the text that answers my questions, providing the page number where that text is located within the given document.

    Thank you.

  145. 145
    hrun0815 says:

    You couldn’t make this stuff up. Really.

    Well spotted, DNA_Jock. Well spotted.

    I simply put Dio’s posts that refer to published work in my mental TL;DR category (which is getting more and more crowded here on UD).

    With this it is also much easier to understand Dio’s disdain in getting some information how to effectively run a project like the one he claims to be working on. Clearly there is no honest interest in the underlying science (considering the multiple points raised by me and others) nor in how to effectively build software relevant to biology.

    Still, the whole charade seems puzzling to me.

  146. 146
    Dionisio says:

    #162 addendum

    Please, be aware that the information you provide may trigger newer questions.

    Basically, you may think like a systems analyst trying to write programming specs. I will be playing the role of a programmer trying to understand the detailed tech specs you write.

    Thank you.

  147. 147
    DNA_Jock says:

    Dionisio,
    My offer, originally made @140, still stands:

    Dionisio,

    when is Nat10 produced for the case of the discussed paper? what triggers that gene expression in relation to the discussed paper? what amount? or is it produced constantly? or is it produced for other processes and just happen to be available for the discussed process too?

    I have an offer for you. I will provide the answers (including references) to these questions for free, if you first provide the URL for the text that you pasted into comment 107.

    [Emphasis added]
    For additional questions, my usual consulting rates will apply. As has been noted elsewhere, you may find engaging a collaborator more cost-effective.

  148. 148
    Dionisio says:

    #165 DNA_Jock

    Does that mean that you’re willing to leave my questions publicly unanswered in this forum?

    If that’s your choice, it should be respected.

    No one has the right to make you answer any questions here.

    Specially if you don’t know the answers, which it’s not your case, right? 🙂

    Have a good weekend.

    O.

    PS. You know very well that the link to the referred paper was provided in my post.
    The information you wanted was available to anyone who read my post. Your request was part of your agenda in this blog. Don’t pretend to be so innocent now. Nice try, but it failed. 🙂

  149. 149
    DNA_Jock says:

    Oh, Dionisio,

    #165 DNA_Jock
    Does that mean that you’re willing to leave my questions publicly unanswered in this forum?
    If that’s your choice, it should be respected.

    How nice of you.

    No one has the right to make you answer any questions here.

    I agree with you, but you might want to let Barry know (LNC, anyone?) (ggg)

    Specially if you don’t know the answers, which it’s not your case, right?
    Have a good weekend.
    O.

    Not quite sure what that means.

    PS. You know very well that the link to the referred paper was provided in my post.
    The information you wanted was available to anyone who read my post.

    Wrong, Dionisio. You still have not stipulated the source of the text that you cut and pasted. Please re-read my offer carefully.

    Your request was part of your agenda in this blog. Don’t pretend to be so innocent now.

    My offer was designed to present you with a dilemma, as I explained quite openly to hrun0815 in 161. So far, you have managed to impale yourself on both horns. That’s quite the feat.

    Nice try, but it failed.

    Au contraire, mon petit ami, au contraire

  150. 150
    DNA_Jock says:

    Hrun0815

    Still, the whole charade seems puzzling to me.

    It’s a game of “Why don’t you/Yes but”.

    The Berne-approved game-breaking response is “Wow, that is an interesting question. What do you think the answer is?, which seems justified at this stage.

    Eagerness to play this game implies a failure to move out of the “I’m not OK” life-stage. Oh well.

  151. 151
    Dionisio says:

    #166 addendum

    DNA_Jock

    Which of these cases contributed more to your decision?

    1. Post #162?
    2. Post #164?
    3. Both posts combined?
    4. None of the above?
    5. Something else? Please specify______ (optional)

    Just having fun here… 🙂

  152. 152
    Dionisio says:

    DNA_Jock

    Ty umnitsa, prosto molodets!

    🙂

    PS. I recall someone suggested a while ago that some of the interlocutors here in this blog could be cover agents working for the blog owners, constantly saying obnoxious things in order to test some of the frequent commenters. Could that be possible? That idea doesn’t make much sense, but who knows?
    🙂

  153. 153
    DNA_Jock says:

    Wow, those are interesting questions. What do you think the answers are?

  154. 154
    Dionisio says:

    #167 DNA_Jock

    Not quite sure what that means.

    Sorry, there was a huge grammar mistake, that most certainly rendered my statement totally unintelligible. Let me correct it for you:

    “Specially if you don’t know the answers, but that is not your case, is it?”

    Is that more clear now?

    🙂

  155. 155
    Dionisio says:

    DNA_Jock

    Let me rephrase it, in case you still didn’t understand it well:

    You know very well that the link to the referred paper was provided in my post #107.
    The information you requested is available to anyone who read my post #107 (until the last time I verified it).
    Your request was completely unnecessary, therefore your complaints are unjustifiable. No idea why you made such a big deal out of that. Nice try, but it failed. Try better next time. 🙂

    🙂

  156. 156
    Dionisio says:

    Is it possible that some interlocutors in this blog are cover agents, hired to entertain the rest of us, pretending to say obnoxious things, just to provoke more heated debates, which supposedly may increase the visitors count and the number of registered commenters?

    That idea seems a little senseless, but who knows?

  157. 157
    DNA_Jock says:

    Dionisio:
    You know very well that the link to the referred paper was provided in my post #107.

    And I have never, ever written anything to suggest otherwise.

    The information you requested is available to anyone who read my post #107 (until the last time I verified it).

    Just as wrong as the last time you said it. I have been asking you to provide the URL from which you extracted the text that you pasted into post 107. If that link is where you copied the text from, then all you need to do is say so.

    Let me rephrase it, in case you still didn’t understand it well:

    Was the text in post 107 copied from the web page linked to in post 107?

    If not, then where was it copied from?

    Your request was completely unnecessary, therefore your complaints are unjustifiable.

    You can read 161 for an explanation of the motivation behind my offer. I am not complaining at all. More like pointing and laughing, I’m afraid.

  158. 158
    Dionisio says:

    DNA_Jock

    Since your buddy hrun0815 has been so ineffective* in helping you, maybe other comrades and fellow travelers could give it a try too? wouldn’t you invite them to step in and give you a hand?

    🙂

    (*) even your buddy hrun0815 publicly admitted that he didn’t understand your senseless request. Here’s what he wrote to you in his post #143:

    I don’t understand. I believe he [Dionisio] did provide the URL. The quote is taken directly from PubMed (or PLOS or PMC).
    Did you [DNA_Jock] mean a different post?

  159. 159
    DNA_Jock says:

    LMAO, Dionisio.

    Did you notice my response to hrun0815 at #144, i.e. the next post?

    hrun,
    I would like Dionisio to confirm the specific URL that he used to copy the text he used in 107. If it was the pubmed link he provided in that post, then answering will be really easy…

    Really easy, and yet you seem strangely reluctant to answer. Curious that. Notice also my explicit acknowledgement that you did provide a link to pubmed, making your 166 and 173 look kinda dumb.

    hrun0815 understood my explanation @144, but he did not understand why you refused to respond, saying @148

    What prevented Dio from just C/P the PubMed link from 107 and then get the answers he was supposedly looking for? And even if he was not actually looking for those answers, why not just C/P and pretend that you are? Why repeat the endless description of his paper collection process?

    He did understand my ‘reveal’ @161 too, responding

    Well spotted, DNA_Jock. Well spotted.

    So I’m quite confident that hrun0815, along with anyone else with the stamina to wade through your spam, understands just fine. Or they could just read #161.
    You couldn’t make this stuff up. Indeed.

  160. 160
    Dionisio says:

    DNA_Jock

    Of course your comrades will always agree with you at the end, because y’all respond to a common party line. 🙂

    Don’t worry about answering the questions I asked AVS (apparently he had not answered yet). The answers are most probably in the same paper or in other papers. Just have to locate and highlight them.

    I’m not specially interested in those answers at this point, because they won’t make a difference in the current phase of my project, which has to do with the proof of concept for the approach I use in order to organize the gathered papers online. Perhaps later some potential users of the method might be interested in having those particular questions answered. They’ll figure out a way to obtain the info they want. Rest assured that they won’t need your help for that.
    🙂

  161. 161
    Dionisio says:

    DNA_Jock

    Would you mind to explain why you are so afraid to answer such easy questions, which just require a little online search?
    Maybe your comrade AVS hasn’t responded yet because he’s on vacation or out of town?
    But you can’t use those excuses, because you’re still writing in this blog.

  162. 162
    Dionisio says:

    DNA_Jock

    Again, I have to admit it:

    Ty umnitsa, prosto molodets!

    🙂

  163. 163
    Dionisio says:

    The Hsp90 Cochaperones Cpr6, Cpr7, and Cns1 Interact with the Intact Ribosome

    doi: 10.1128/EC.00170-14

    The abundant molecular chaperone Hsp90 is essential for the folding and stabilization of hundreds of distinct client proteins.

    Hsp90 is assisted by multiple cochaperones that modulate Hsp90’s ATPase activity and/or promote client interaction, but the in vivo functions of many of these cochaperones are largely unknown.

    http://ec.asm.org/content/14/1/55.abstract

  164. 164
    Dionisio says:

    Quality control of a cytoplasmic protein complex: Chaperone motors and the ubiquitin-proteasome system govern the fate of orphan fatty acid synthase subunit Fas2 of yeast

    doi: 10.1074/jbc.M114.596064

    For the assembly of protein complexes in the cell the presence of stoichiometric amounts of the respective protein subunits is of utmost importance.

    A surplus of any of the subunits may trigger unspecific and harmful protein interactions and has to be avoided.

    A stoichiometric amount of subunits must finally be reached via transcriptional, translational and/or post-translational regulation.

    http://www.jbc.org/content/ear.....114.596064

  165. 165
    Dionisio says:

    Concerted Action of the Ribosome and the Associated Chaperone Trigger Factor Confines Nascent Polypeptide Folding

    DOI: http://dx.doi.org/10.1016/j.molcel.2012.07.018

    How nascent polypeptides emerging from ribosomes fold into functional structures is poorly understood.

    http://www.cell.com/molecular-.....12)00645-4

  166. 166
    Dionisio says:

    DNA_Jock

    Here’s more of the same ‘medicine’ for you and your buddies:

    http://www.uncommondescent.com.....ent-542513

    Enjoy it!

    🙂

  167. 167
    Dionisio says:

    AVS

    Here’s more of the same bitter ‘syrup’ for you and your comrades:

    http://www.uncommondescent.com.....ent-542560

    Enjoy it!

    🙂

    PS. At least now you should know why I highlight text the way I deem appropriate.

    Feel free to post references to the descriptions of any of the procedural issues still unexplained in the given papers. Most probably some readers will appreciate it.

  168. 168
    AVS says:

    Don’t get your panties in a wad Dio.
    Like I said, I’m merely trying to help you!
    I asked why you highlight certain things, you respond with “I try and highlight some of the issues that are not explained in the given paper.”
    The fact is though, that most of what you have highlighted in the past, probably the vast majority, is explained in the papers you cite.
    You don’t know this most likely because you simply skim the abstracts for what you think are unanswered questions, don’t have access to the majority of the full papers, and don’t read or understand the ones you do have access to.
    I am just letting you know that if a question is raised in the abstract of a scientific paper, it is (more often than not) answered in the subsequent pages.

    My assumption is that your whole “project” is a load of crap, and you simply were highlighting things in an attempt to show how little we actually know about biology.
    But in fact, you were highlighting questions researchers have recently answered.
    Let me know if you would like more assistance.
    I’ll even give you a hint, if you want unanswered questions, focus on review articles.
    The more recent the better.

    Have a nice day on cloud-9!

  169. 169
    Dionisio says:

    AVS,
    I explained with much details why I highlight som text. If you don’t want to accept my explanations, that’s your problem.
    You’ve disappointed many folks here who were hoping you will come back and respond my questions to you in posts #129-133, 137,138,… Did you miss those posts?

    Go ahead, try again. But read more carefully next time. Many people reading this thread might get the wrong impression about you, and think you know much less than you claim. C’mon don’t let your buddies down, specially now, when they’re all on the run and would use any help they could get. 🙂

    Go back to those posts I mentioned above, which you have ignored so embarrassingly, and answer those questions. Don’t forget that there are more complex questions awaiting to be answered. I started from the easiest ones for you to find the answers for. The questions that might follow could be really challenging. But we’ll look at that later.
    However, the good news is that most answers are in the same papers, but most are paywalled, hence can’t access them. So just provide the link to the paper, the page number (from-to), and voilà you’re done. You see? pretty simple. Why didn’t you answered them right away, instead of ignoring them?

    Ok, third time: answer the questions I asked you in the above mentioned posts. Get serious for once.

    🙂

  170. 170
    AVS says:

    Dio, why on Earth would I answer your questions when on numerous occasions, others have offered to answer them and you were incapable of meeting a simple requirement?
    Not only that, but you just admitted in your post 178 that you are not even interested in the answers.

    The game is up. You’re “project” BS is idiotic.
    Just call it what it is:
    You point out things we don’t know yet in a pathetic attempt to show evolutionary biology in a bad light.
    Or maybe you’re just a comic-genius because, man, it’s funny as hell to watch you run around like a chicken with its head chopped off.

  171. 171
    Dionisio says:

    #188 AVS

    You’re “project” BS is idiotic.

    Did you mean “your” but mistakenly wrote “you’re” which stands for “you are”?

    Should you go back to elementary school to learn basic grammar?

  172. 172
    Dionisio says:

    AVS,

    The posts #162 164 166 169 170 172 173 176 178 179 180 explain clearly that the alleged ‘offer’ to answer my questions turned false because your buddy didn’t know the answers, even after I provided the hint that they might be in the same paper.

    Obviously you and your comrades don’t seem interested in serious discussions, but I’ve listed the post numbers here intentionally, as sequential references for anyone reading this thread to see what really happened here. 🙂

    I have stated on several occasions in different threads within this blog that the information provided in the research reports shed more light on the biological systems, confirming their functional complexity. Every report makes it more difficult for the officially accepted theories to explain OOL.

    My posting and highlighting was explained clearly in some of my comments within this thread and in other threads. However, you obviously avoided getting into the details of what I explained. That’s your problem.

    Your motives to participate in this blog are very visible in most of your posts.

    Why don’t you want to answer my easy questions, which as you said are already explained within the same given papers? Why?

    Are you afraid of digging deeper into more details? Why?

    Can you explain your attitude and behavior here, publicly?

  173. 173
    Dionisio says:

    #188 AVS

    The game is up.

    What game? the ‘dirty’ one you and your comrades try to play in this blog every day?

    Why do you always quit when you see yourself cornered by questions you don’t want to answer?

    Why don’t you want to answer them?

    Are you afraid of certain revelations that might become more clearly visible to all readers here if the discussions get deeper into complex areas that none of us will be able to handle, but questions will keep coming in?

    Is that what really concern you and your comrades?

    The deeper research penetrates into the biological systems the more light is shed on the elaborate cellular and molecular choreography that is orchestrated in sometimes very intriguing ways.

    Do not be afraid of that. Quite on the contrary, enjoy it!
    Aren’t you excited to see the unending revelation of the ultimate reality? There is true wonder beyond the visible horizon. Let’s all enjoy it together. These are fascinating times to watch closely what’s going on in science research.

    Please, think seriously about this. Don’t let this opportunity to pass by.
    This is the time, this is the best time. Now.

  174. 174
    Dionisio says:

    AVS,

    Remember that you’re not the only reader of these discussion threads. 🙂

  175. 175
    Dionisio says:

    AVS,

    The admin and moderators of this blog must love you and your comrades for creating additional traffic! Do you work for them by any chance? Did they hire you for that purpose? Are you just pretending? 🙂

  176. 176
    DNA_Jock says:

    Dionisio,
    Here’s a question for you to ponder on while I formulate a response to your comments:

    When you do your bolding thing, why do you give credence to the authors` statement that “X is unknown”? is it because

    1) It’s a statement “against interest”
    2) The authors are authorities in this field
    3) There is a consensus amongst scientists that “X is unknown”
    4) The statement is made in a peer-reviewed article
    Other, please specify…

    Please think carefully before responding.

  177. 177
    Dionisio says:

    AVS,

    I am just letting you know that if a question is raised in the abstract of a scientific paper, it is (more often than not) answered in the subsequent pages.

    I’ve explained to you clearly in previous posts why that’s not accurate. The paper may answer -as far as biologists may expect- the main issue raised in the title and in the abstract, but it does it in a way that assumes the reader knows certain things which I don’t know. Additionally, their descriptions may lack the granularity or detail level that is required in order to develop an interactive animation that does not leave obvious questions unanswered, as it’s the case with most animations we see online.

    They try to represent certain processes in such a reductionist manner that one ends up with more questions at the end of watching such animations. In addition to that, one can only watch passively such animations. No interaction is possible. No way for on to affect the process by introducing additional information, modifying the conditions.

    My colleagues and I want to avoid that situation as much as possible. First, the user should be able to play the animation in different scenarios under different conditions and trying different choreographic approaches, where each class of object involved in a given story can be preset with physical properties and functional attributes that may affect their behavior and interaction with surrounding objects and environment.

    As you can imagine, that’s not an easy task, but it’s achievable. The project has various chronological phases, one of which is designing a practical methodology for gathering and organizing the input information. That’s the area I’m working on now. This is why I’m more interested in the way the information is located, marked up, reviewed, selected, stored, organized, sorted, tagged, interwoven, multidirectional linked, etc. If you have used Zotero and Mind Meister tools you might understand what I’m trying to explain to you.

    Please, make some serious effort to understand this. Any serious suggestions or comments are welcome. This is still a ‘work in progress’ situation, with some ‘proof of concept’ tasks included too.

    If you choose to continue in your stubborn attitude to decline my invitation to engage in a serious discussion, then too bad.

    [Monday, Jan. 19, 2015]

  178. 178
    Dionisio says:

    #194 DNA_Jock

    I think in this case the correct answer is ‘none of the above’.

    I have responded your valid questions in several posts within this thread. Please, review those posts and ask specific questions about what I wrote in them. You may want to quote which specific part of my explanations is not clear to you, and I will gladly try my best to clarify it (despite my language limitations and my poor communication skills). If you point to a real error in my explanation, I will try and correct it ASAP, giving you the credits for finding the mistake and for alerting me about it. I will appreciate any valid constructive correction because I get benefited from it, because that’s an important part of my learning process too.

    Maybe that interaction will lead us to a newer, more interesting level of discussion. Obviously, there are certain aspects of my work that I won’t be in condition to reveal at this point, because they are not of public domain yet, but I will carefully try to explain as much as I’m allowed to, at least in general terms and using examples that are available to all.

    If you can’t find my explanations, I could list the post #s for you. Just let me know how you want to proceed with this. But please, be open minded, think outside the box.

    Thank you.

  179. 179
    DNA_Jock says:

    Dionisio,

    My question included “Other, please specify”. By replying “none of the above”, you imply that you have NO reason for attaching any credence to the authors` statements, making your grand project, err, pointless.

    Love it.

  180. 180
    DNA_Jock says:

    Dionisio,
    AVS, hrun0815 and myself have had your number from the very get-go. It is truly delightful that you don’t even realize that you are in a hole. Keep digging. As AVS summed it up @186

    My assumption is that your whole “project” is a load of crap, and you simply were highlighting things in an attempt to show how little we actually know about biology.
    But in fact, you were highlighting questions researchers have recently answered.

    I made you an offer (@140 , repeated @165)

    Dionisio,

    when is Nat10 produced for the case of the discussed paper? what triggers that gene expression in relation to the discussed paper? what amount? or is it produced constantly? or is it produced for other processes and just happen to be available for the discussed process too?

    I have an offer for you. I will provide the answers (including references) to these questions for free, if you first provide the URL for the text that you pasted into comment 107.

    [Emphasis added]
    For additional questions, my usual consulting rates will apply. As has been noted elsewhere, you may find engaging a collaborator more cost-effective.

    As AVS notes in #188, you still have not met my simple requirement, viz:
    answer the question

    Was the text in post 107 copied from the web page linked to in post 107?
    If not, then where was it copied from?

    You have also admitted (#178) that you are not interested in hearing the answer.
    You have, OTOH, claimed that I am “so afraid to answer such easy questions”, that I don’t have the answers, etc. etc.
    You write:

    The posts [snip] explain clearly that the alleged ‘offer’ to answer my questions turned false because your buddy didn’t know the answers, even after I provided the hint that they might be in the same paper.

    You did provide the “hint” that they might be in the same paper. Hilarious! Actually, I do know* the answers, and they are NOT in that paper.

    *to the extent that they are known.

    As I explained to hrun0815 @161, the purpose of my offer was to present you with a dilemma, wherein you would either have to admit that your bolding schtick was dishonest, or admit that you were uninterested in hearing answers to your numerous questions. Thanks to your spluttering evasions, no-one is in any doubt as to the source of your text for #107, and you have also admitted (@178) your lack of interest in hearing your questions answered. You managed to impale yourself on both horns – I`m impressed.

    But here’s the funny thing, even when your “bolding unanswered questions” schtick is honest, and avoids the problem of bolding questions which ARE answered in the same paper, it still doesn’t make the point you that think it does:

    Your argument, and your bolding unanswered questions schtick, rests on the idea that the more unanswered questions there are, the more biological sciences are in trouble. This is hilariously wrong. It is common knowledge that good science leads to an increase in the number of unanswered questions, and an increase in knowledge, simultaneously. I pointed Andre to “Zen and the Art of Motorcycle Maintenance” for an example of this; if you want a more academic treatment of the same subject, read Kitcher’s “Abusing Science”.

    Let me give you a (cartoon) example:

    Before radioactivity was discovered, there were no unanswered questions in nuclear physics. There was a disagreement between physicists on the one hand, and geologists and biologists on the other, about the age of the earth. The discovery of radioactivity “solved” the age of the earth problem (vindicating Darwin, fyi), but it introduced thousands of new questions to be answered – the half-lifes and modes of decay of every single nuclide.

    Your spamming of various threads at UD is entertaining (to me, at least: UBP`s view may differ); you imply that you are doing this to give the reality-based posters “a taste of their own medicine”. You evidently think that these posters (and their comrades and fellow travelers [gggg]) are “spamming” when they provide references to support their claims. You do not seem to understand what “evidence” is. Don’t worry, it’s a common failing amongst the ID crowd.

    Take-home:
    Biology is complicated. Biologists know this. If you chose any ten articles at random from pubmed, they would, in net, INCREASE our knowledge and understand of biology, and at the same time they would INCREASE the number of unanswered questions. That’s not a bug, it’s a feature. It’s how science works. There are over 24 million articles in pubmed. Going through all of them and manually bolding the text you find provocative is going to take you a while…
    Keep up the good work.

    My offer @165 still stands, if you are interested.

  181. 181
    Silver Asiatic says:

    DNA_Jock

    Biology is complicated. Biologists know this.

    This statement is wildly inconsistent with The Greatest Theory Known to Mankind. Natural selection and random mutations – remember? That’s what Dionisio brings to light. Now you’ve admitted it. You claim that biologists actually know that the natural world is “complicated”, even though they try to explain the origin of the entire biosphere from their own, idiotically simplistic theory.

    If you chose any ten articles at random from pubmed, they would, in net, INCREASE our knowledge and understand of biology, and at the same time they would INCREASE the number of unanswered questions.

    You keep slipping here, DNA_Jock – wrong answer! You should have said: “if you choose any ten articles they would, absolutely, confirm every prediction made in evolutionary biology and what we need to fully validate the theory decreases”.

    The general topic at UD is that of origins, not necessarily of biological minutia.

    That’s not a bug, it’s a feature. It’s how science works. There are over 24 million articles in pubmed.

    I think we know how science works:
    “There are no weaknesses in evolutionary theory”. “Evolution is the most highly confirmed and validated theory in the history of science”.
    “Evolution is more certain than gravity”.

    A brief review of Dionisio’s posts reveals that almost nothing is said about the evolutionary origin of the organisms and functions under discussion.

    If you guys want to laugh at something, you might start there.

  182. 182
    DNA_Jock says:

    Silver Asiatic writes:

    DNA_Jock

    Biology is complicated. Biologists know this.

    This statement is wildly inconsistent with The Greatest Theory Known to Mankind.

    Yes, my statement is wildly inconsistent with your strawman version of evolutionary theory, TGTKtM, so either I am wrong or your strawman is inaccurate. Wow, there’s a doozy…

    A brief review of Dionisio’s posts reveals that almost nothing is said about the evolutionary origin of the organisms and functions under discussion.
    If you guys want to laugh at something, you might start there.

    Well, in general Dionisio’s posts are carefully edited to omit the answers to the questions he highlights. The articles he cites may or may not address the evolutionary origins of the biological activities they discuss. They don’t discuss the cosmological origin of carbon either. Your point?

  183. 183
    AVS says:

    Ok, Dio, let me help you some more. First clear some things up for me, quick and concise please.

    What exactly do you envision being in the videos you ultimately produce?
    Do you plan on running molecular simulations to produce your videos?
    How long do you think the video will end up being?
    What kind of resolution are you planning on? Atomic resolution? Or will it simply be animations?

  184. 184
    Dionisio says:

    #197 DNA_Jock

    My question included “Other, please specify”. By replying “none of the above”, you imply that you have NO reason for attaching any credence to the authors` statements, making your grand project, err, pointless.

    You’re wrong. Again.

    You only listed 4 numbered options.

    When I wrote “None of the above” I meant the 4 numbered options you provided.

    Perhaps, in a way, I was saying about the same as your “Other, please specify”, but expressed differently.

    Almost my entire post #196 was devoted to graciously answer your post #194, specially the “…, please specify” request.

    Did you read my comments in post 196? Apparently you didn’t read it carefully, because it seems like you didn’t realize I was replying to your “Other, please specify” statement.

    As usual, you jumped into premature conclusions, and wrote whatever you wanted to write.

    Someone suggested that some interlocutors in this blog are paid agents of the blog administration, to pretend being silly and thus provoke heated arguments that could attract more visitors to the site.

    I don’t quite understand that intriguing suggestion, but sometimes I wonder if it is true and you along with your comrades are one of those paid cover agents. If that’s the case, then you’re doing it very well. Congratulations!

    But maybe that’s not your case.

    Anyway, I have to admit that “ty umnitsa, prosto molders!”

  185. 185
    Silver Asiatic says:

    DNA_Jock

    Yes, my statement is wildly inconsistent with your strawman version of evolutionary theory, TGTKtM, so either I am wrong or your strawman is inaccurate. Wow, there’s a doozy…

    We’re on the lookout for the real version of evolutionary theory – the one that has no weaknesses and which offers precise and accurate predictions with each new finding in the data. It’s the version of evolutionary theory that shows, with detail, the power of natural selection in the development of genetic regulatory mechanisms, for example.

    But the problem is within the biological community itself, not with me. We’ve seen enough posts from biologists who propose a “third way” for evolution or alternatives to neo-Darwinism to know that the “real version” of evolutionary theory doesn’t work.

    With that, I might say that your version of evolutionary theory could be considered a strawman as well, especially if you’re proposing it as highly certain and irrefutable.

    The articles he cites may or may not address the evolutionary origins of the biological activities they discuss. They don’t discuss the cosmological origin of carbon either. Your point?

    If you’re saying that ideas on biological evolution are about as certain and equivalent to the cosmological origin of carbon, that would be saying something.

    Supposedly, nothing in biology makes sense except in the light of evolution. But the articles somehow avoid even mentioning evolutionary origins of highly complex features.

    My point is that biologists struggle to explain how certain biological activities even work in living creatures they can observe today and yet at the same time they claim that evolutionary theory explains the origin of all of these things from the deep historical past.

    It’s convenient that they don’t have to actually explain how they evolved.

    Dionisio’s point is pretty obvious for most ID supporters. There are hundreds of examples of biological features that are inexplicable in the current evolutionary model. Most papers don’t even try to explain the origin of what they struggle to describe. When they do attempt to explain the evolutionary path, it’s even more laughable than if they kept silent about it.

  186. 186
    Dionisio says:

    #201 AVS

    Buddy, your misinformation reveals that you still haven’t done your homework reading carefully my posts # 189-193, 195.

    I kindly suggest you better get to work and learn your lesson before you can start whining again.

    BTW, FYI – I write the post #s so that all the readers of this thread can follow this senseless discussion accurately, without missing any detail, thus they can have a more educated opinion about the discussed subject.

    🙂

  187. 187
    AVS says:

    So Dio, you aren’t looking for comments and suggestions on your project, or is this whole project thing just a steamy pile of cow chips?

    Your choice.

  188. 188
    Dionisio says:

    #202 correction:

    Prosto molodets!

  189. 189
    DNA_Jock says:

    Silver Asiatic wrote:

    We’re on the lookout for the real version of evolutionary theory – the one that has no weaknesses and which offers precise and accurate predictions with each new finding in the data. [snip] …I might say that your version of evolutionary theory could be considered a strawman as well, especially if you’re proposing it as highly certain and irrefutable.

    Yup. Just as I thought. That would be your strawman version of evolutionary theory, “TGTKtM”. It bears no relation whatsoever to actual evolutionary theory, which is always provisional, always refutable.

    My point is that biologists struggle to explain how certain biological activities even work in living creatures they can observe today and yet at the same time they claim that evolutionary theory explains the origin of all of these things from the deep historical past.

    Yes, biologists work to understand biology, and (to date) MES is the best explanation we have. Do you have a more parsimonious and predictive explanation?

    There are hundreds of examples of biological features that are inexplicable in the current evolutionary model.

    ^^ This is the central assertion of the ID movement. Your problem is the elision from the fact that there are features that have not yet been explained to the unsupported assertion that these features are “inexplicable”. Science has a pretty impressive track record here.

    Most papers don’t even try to explain the origin of what they struggle to describe.

    And they don’t even try to explain the origin of carbon, either. Their subject matter is molecular biology, rather than evolutionary biology, or cosmology. Capiche?

    When they do attempt to explain the evolutionary path, it’s even more laughable than if they kept silent about it.

    With the notable and unique exception of gpuccio (who understands a fair amount of biology, but has a blind spot regarding Texas SS), every critique of evolutionary explanations that I have read on this site betrays on a woeful ignorance of biology: kairosfocus on “islands of function”, Andre on PCD, News on…err, well …News on anything.

    Even more revealing, however, is the lack of understanding of the nature of science and how research is conducted. Given Dionisio’s non-response @196, would you like to try your hand at answering the question I posed to Dionisio @194?

  190. 190
    Silver Asiatic says:

    DNA_Jock

    It bears no relation whatsoever to actual evolutionary theory, which is always provisional, always refutable.

    What I'm talking about may 'bear no relation whatsoever' to your version of evolutionary theory. That's certainly fine with me. It just means we're talking about different things and it will be difficult to continue the discussion in that case.

    Yes, biologists work to understand biology,

    You agree – they struggle to explain the function things they claim to know the origin of.

    and (to date) MES is the best explanation we have.

    It’s interesting to see how modest an evolutionary-promoter becomes at times. ET is merely “the best we have”. Once again, you back away from the grand claim. You should say that “it is the only theory of biological origins that is correct”.

    Do you have a more parsimonious and predictive explanation?

    Some aspects of nature indicate evidence of having been designed by intelligence.

    ^^ This is the central assertion of the ID movement. Your problem is the elision from the fact that there are features that have not yet been explained to the unsupported assertion that these features are “inexplicable”.

    It’s not an assertion, it’s a prediction.

    Science has a pretty impressive track record here.

    Impressive yes, but not without room for critique.

    And they don’t even try to explain the origin of carbon, either. Their subject matter is molecular biology, rather than evolutionary biology, or cosmology. Capiche?

    They don’t try to explain the evolutionary origin because they can’t. They can’t because they don’t even know how to explain the observation. Yes, I capiche.

    Ann Gauger offers a nice summary of what we see from evolutionary biologists:

    The evolutionary view attributes any observed similarity to evolutionary relatedness, and explains all biological structures as the result of purely natural evolutionary processes. This is the case even for complicated biological apparatus like programmed cell death, the cell cycle system, chromatin remodeling machinery, structures like the nuclear envelope, or for DNA sequences like the Y chromosome MSY (see above).
    Design language unintentionally pervades mainstream papers despite a bias against intelligent design. It’s so noticeable that articles have been written urging scientists to avoid teleological language (that is to say, design language) and use more evolutionary language. In other words, more spin.
    http://www.uncommondescent.com.....e-as-well/

    More spin. It's a critical part of evolutionary biology itself.

    With the notable and unique exception of gpuccio (who understands a fair amount of biology, but has a blind spot regarding Texas SS), every critique of evolutionary explanations that I have read on this site betrays on a woeful ignorance of biology:

    I guess you think Fodor, Denton, Behe, Stuart Newman Gauger, Axe, Minnich, Snoke, Giertych are ignorant of biology.

    Given Dionisio’s non-response @196, would you like to try your hand at answering the question I posed to Dionisio @194?

    “When you do your bolding thing, why do you give credence to the authors` statement that “X is unknown”?”

    I can’t answer for Dionisio but he’s probably just reacting against the absurd claims we hear (although less frequently, I admit) from evolutionists that there is basically nothing in biology that is a mystery at all. Modern evolutionary theory basically explains it all. When we see papers pointing to unknown aspects of biological life, it’s an indication that the evolutionary claims are over-stated.

    If we arrive at a point where more biologists are willing to admit, modestly (as you’ve done) that evolutionary theory is merely “the best we’ve got” – that’s a huge step forward. We’re not there yet though.

  191. 191
    Dionisio says:

    #205 AVS

    First read carefully post # 204 and then come back with more questions.

    BTW, are you also a paid cover agent working for the admin of this site, pretending to be stubbornly unpleasant, so that the discussions turn senseless, but heated enough to attract the attention of trashy talk show audiences, thus increasing the site traffic?

    Or you do all that voluntarily?

    Is your constant foul language included in your contract?

    Or is it part of your party line?

    🙂

  192. 192
    AVS says:

    Why would I come back with more questions when you can’t even answer those few basic questions?

    I haven’t even used foul language (recently) =)
    I just calls ’em as I sees ’em.

    And what I see is your inability to answer basic questions about your “project” because this project doesn’t exist anywhere but in Dio’s mind.

    If you can come up with an answer to any of those basic questions about your project (which you have been working on for who knows how long now(it’s been over 7 months since your first “third way” post)), I will be very surprised.

    Like I said, game over player 2.

  193. 193
    Dionisio says:

    AVS,

    The project I’m working on is not intended for people like you or your comrades, hence I careless what you think about it. Your opinion on the subject doesn’t make any difference. It’s totally irrelevant.

    This is for you:

    http://www.uncommondescent.com.....ent-542958

    Ty umnitsa. Prosto molodets !

    🙂

  194. 194
    AVS says:

    Good chat Dio, and good luck on your project! Can’t wait to see the results!

    I guess there’s more than one way to keep an idiot busy.

  195. 195
    Dionisio says:

    AVS

    Can’t wait to see the results!

    You won’t see anything. My project is not available to you or your comrades. It’s restricted access by invitation only. Anyway, you wouldn’t enjoy it.

    🙂

  196. 196
    Dionisio says:

    AVS

    Are your frequent personal attacks required in order to maintain your party affiliation?

  197. 197
    Silver Asiatic says:

    DNA_Jock

    When you do your bolding thing, why do you give credence to the authors` statement that “X is unknown”?

    Just to follow up, when the author states that the “function of X” is unknown then by implication we should conclude that “the evolutionary origin of X is unknown”.

    That shouldn’t be a problem for anyone. Now if we find hundreds of examples that fit the above model, we’d find hundreds of examples of where the evolutionary origin of organisms is unknown.

    I can’t go farther answering your question to Dionisio. But if I did my own “bolding thing” in biological texts, I would follow the lead found here (from Ann Gauger’s remarks cited earlier):

    Design language unintentionally pervades mainstream papers despite a bias against intelligent design. It’s so noticeable that articles have been written urging scientists to avoid teleological language (that is to say, design language) and use more evolutionary language.

    Scientists have been urged to remove design language from their articles, so it is interesting to see where it appears.

    Dionisio highlights that kind of teleological language frequently in his posts.

    “We further demonstrate that Rqc2p recruits alanine- and threonine-charged tRNA to the A site and directs the elongation of nascent chains independently of mRNA or 40S subunits.”

    Ribosomes stalled on aberrant mRNAs engage quality control mechanisms that degrade the partially translated nascent polypeptide.

    mechanism linking translation and protein degradation that targets defective proteins immediately after synthesis, while ignoring nascent chains in normally translating ribosomes

    human cells adopt unique strategies and recruit distinct trans-acting factors

  198. 198
    DNA_Jock says:

    Silver Asiatic:

    What I’m talking about may ‘bear no relation whatsoever’ to your version of evolutionary theory. That’s certainly fine with me. It just means we’re talking about different things and it will be difficult to continue the discussion in that case.

    So you are arguing against a cartoonish strawman of your own creation. To each his own, I guess.

    Yes, biologists work to understand biology,

    You agree – they struggle to explain the function things they claim to know the origin of.

    Ha ha, nice try, SA. That is not what I said.

    It’s interesting to see how modest an evolutionary-promoter becomes at times. ET is merely “the best we have”. Once again, you back away from the grand claim. You should say that “it is the only theory of biological origins that is correct”.

    You seem strangely eager to put words in my mouth. I guess that arguing against a fictional adversary brings you more satisfaction. I understand.

    Do you have a more parsimonious and predictive explanation?

    Some aspects of nature indicate evidence of having been designed by intelligence.

    So “designed by intelligence” is your idea of a parsimonious and predictive explanation?

    This is the central assertion of the ID movement. Your problem is the elision from the fact that there are features that have not yet been explained to the unsupported assertion that these features are “inexplicable”.

    It’s not an assertion, it’s a prediction.

    No, the corresponding prediction would be the underwhelming “these features will not be explained by evolutionary biology”. This is where Science’s rather impressive historical track record comes in.
    God of the Gaps, anyone?
    Does your theory offer any testable predictions?

    With the notable and unique exception of gpuccio (who understands a fair amount of biology, but has a blind spot regarding Texas SS), every critique of evolutionary explanations that I have read on this site betrays on a woeful ignorance of biology:

    I guess you think Fodor, Denton, Behe, Stuart Newman Gauger, Axe, Minnich, Snoke, Giertych are ignorant of biology.

    What a sad list.
    Fodor, Gauger, Axe, and Snoke are ignorant of biology.
    Please provide the links to the critiques by Denton, Behe, Minnich or Giertych at Uncommon Descent and I’ll see if they betray ignorance. Denton and Behe do have a history of confirmation bias…
    Not sure why you would bring up Stuart Newman. He’s a full-on ‘evolutionist’. Have you been misled by Cornelius Hunter’s quote-mining, perhaps?

    I’ll see your list and raise you Szostak, Hunt, Sulston, and [waves to gpuccio] Walker.

    I can’t answer for Dionisio but he’s probably just reacting against the absurd claims we hear (although less frequently, I admit) from evolutionists that there is basically nothing in biology that is a mystery at all. Modern evolutionary theory basically explains it all.

    Citations for biology researchers, please.

    When we see papers pointing to unknown aspects of biological life, it’s an indication that the evolutionary claims are over-stated.

    But my question to Dionisio @194 was “why do you give credence to the authors` statement that “X is unknown”? That is, why do you believe these authors when they make these statements? Pick all reasons that apply. Don’t be shy – Give it a go.

  199. 199
    Silver Asiatic says:

    DNA_Jock

    Ok, you’re denying that evolutionists (I didn’t limit it to biology researchers) claim that their theory is essentially complete and explains the origin of the entire biosphere on earth.

    Citations for biology researchers, please.

    Ok, I will do the research for you and show what I mean. Keep in mind we argue against evolutionists who say such things as part of their propaganda and not necessarily against biology researchers.

    But my question to Dionisio @194 was “why do you give credence to the authors` statement that “X is unknown”?

    1) It’s a statement “against interest”
    2) The authors are authorities in this field
    3) There is a consensus amongst scientists that “X is unknown”
    4) The statement is made in a peer-reviewed article

    First of all, I don’t give credence to any and all authors statements. I wouldn’t be surprised if they’re lying or delusional – I expect that from the evolutionary biology community.

    I don’t understand #1.
    #2 Evolutionists consider them authorities. You know what would happen if we quoted ‘creationists’
    #3 There are wildly conflicting views in the evolutionary community — except that evolutionary theory (in whatever verion) is correct.
    #4 Like #2 above. Evolutionists cannot dismiss the quote since it comes from their own authorities.

    Does your theory offer any testable predictions?

    Yes, we observe biological functions and we predict that these can be imitated and replicated by intelligent processes and the same cannot be done by unintelligent processes.

  200. 200
    DNA_Jock says:

    Silver Asiatic,

    I didn’t ask you why “evolutionists” give credence to such statements, I specifically asked why do you give credence to such statements.

    Given your view that:

    First of all, I don’t give credence to any and all authors statements. I wouldn’t be surprised if they’re lying or delusional – I expect that from the evolutionary biology community.

    How do you distinguish between the statements that you attach weight to, and the statements that you ignore as being lies or delusions?

  201. 201
    Dionisio says:

    DNA_Jock, AVS, and your comrades:

    Vy umnitsy, prosto molotsy!

    Here’s another sample of the bitter medicine that y’all dislike so much:

    http://www.uncommondescent.com.....ent-543099

    znacznego! pryatnovo apetita!

    🙂

    PS. There are many more samples of the same yucky medicine, and more will continue to appear.

  202. 202
    Silver Asiatic says:

    DNA_Jock

    How do you distinguish between the statements that you attach weight to, and the statements that you ignore as being lies or delusions?

    Of course, statements appear in a variety of contexts with varying levels of support. Statements that are assertions, speculations or various sorts of wishful thinking and story-telling get less weight than statements that are supported by multiple sources of data.

    Evolutionary interpretations get less weight (from me) than mere facts about observations. Statements that include conditional or speculative phrases like “might have evolved” or “may have emerged” or “could have developed” I usually consider to be lies and/or delusions. And that’s what most of evolutionary science is, in my opinion.

    I think we all use filters when reading and I try to discern where there is bias in an evolutionary argument.

    I’ve posted this twice already, but here it is again:

    Design language unintentionally pervades mainstream papers despite a bias against intelligent design. It’s so noticeable that articles have been written urging scientists to avoid teleological language (that is to say, design language) and use more evolutionary language. In other words, more spin.

    Here, Ann Gauger points out that biological language is being scrubbed of certain terminology for fear that it can be interpreted as support for the design inference.

    That’s censorious and manipulative – and a form of lying or false propaganda.

    To continue, it also depends on what I know about the particular evolutionist. I read guys like Richard Dawkins, Jerry Coyne, PZ Myers or Ken Miller as propagandists.

    You may ask: “What can you really know about biology if you don’t trust what the scientists say?”

    Of course, as a non-scientist who cannot do research to audit what is written in papers, everything I see is based on some level of trust.

    But, as mentioned above — if the science refers to observations of existing organisms I give that a higher degree of credibility, but even there with caution. As another extreme, when there is a speculation about how a particular thing “could have” evolved from an imagined ancestor millions of years ago, I give that a far less weight.

    When Dionisio posts items on amazingly complex, existing biological functions that cannot even be accurately described – then I’m not surprised when nobody talks about even how they “could have evolved”.

    When evolutionists here on UD get indignant about the fact that there is no biological literature on the evolution of such things (since they don’t talk about cosmology either), I add that to a growing collection of evidence about what evolutionary theory actually is and how its defenders deal with obvious problems for the theory.

  203. 203
    AVS says:

    “Statements that include conditional or speculative phrases like “might have evolved” or “may have emerged” or “could have developed” I usually consider to be lies and/or delusions. And that’s what most of evolutionary science is, in my opinion.”

    Hahahaha woww.
    Someone is bitter.
    Who pooped in your cheerios, Silver?

  204. 204
    Dionisio says:

    Silver Asiatic

    Well done.

    Apparently they don’t like the fact that science is betraying them by revealing -at a fast pace- so many regulatory networks, signaling pathways, elaborately interwoven molecular and cellular choreographies, orchestrated within the biological systems in ways that can’t be easily explained by unguided processes.

    Perhaps that’s why they get so upset, writing personal attacks in offensive foul language, trying to throw red herrings to distract everyone’s attention onto completely irrelevant issues, while avoiding serious discussions about the growing amount of evidences constantly appearing in the research papers that lead to conclusions they dislike so much? Really don’t know with certainty, but many things point in that direction.

    They even tried to tell us how we should write our posts. That’s beyond ridiculous. Why were they so concerned with my posting style? Could it be that those posts bother them? If that’s the case, let it be. Their problem, not ours. They can always go somewhere else where they won’t find posts written in ways they so dislike. Or simply ignore my posts completely. No one forces them to read anything here.

    This thread, which looked so dormant at its start, has gone beyond the 200 posts, in part because some interlocutors have barked up the wrong trees and whined about some posts they found here, which obviously made them feel uncomfortable.

    Most attempts to engage them into serious discussions fail and turn into squandered time.

    But that’s fine. Let’s keep moving. They ain’t seen nothing yet. The research papers should keep coming with interesting information that must be dissected into details, in order to have a more accurate idea of what’s going on in biology.

    There’s an overwhelming amount of scientific information that keeps growing at a faster pace than it can be analyzed accurately. But new technological advances should help with speeding the multidisciplinary analysis of the growing data.

    🙂

  205. 205
    Axel says:

    Wow! Sounds good, Dionisio.

  206. 206
    Axel says:

    AVS, your #221

    It’s a plain fact, they build up a wonderful edifice of completely gratuitous speculations…. until you backtrack and arrive at the first ‘artistic’ postulation… and then go forward again, pondering each step of the way.

  207. 207
    DNA_Jock says:

    Dionisio,

    Anyone who is any doubt about what you`re doing here can read my 198 and the references therein. My offer at 165 stands.

    Silver Asiatic,

    Thank you for your detailed response @220. Confirmation bias is an interesting phenomenon.

  208. 208
    Dionisio says:

    DNA_Jock, AVS and all your party comrades:

    Serious scientists are working hard, hence more bad news for y’all are coming soon:

    http://www.uncommondescent.com.....ent-543231

    Sorry. Oh, you poor things.

    Is there anything we can do to help you get out of that nightmarish situation you’re getting yourselves in?

    Just let us know. I’m sure many folks here are willing to help you, free of charge, unconditionally, unlike you, who wrote in one of your posts that you offer conditional assistance. Anyway, who needs help from you?

    🙂

  209. 209
    Dionisio says:

    OT

    Just noticed this thread reached 1111 visits and over 225 comments. Not bad for a topic that seemed so ‘nerdy’ and ‘uninteresting’ at the beginning.

    Perhaps hiring* some ‘pretending’ interlocutors to keep the heat on is paying off after all? 🙂

    (*) are they contractors or volunteers?

  210. 210
    Dionisio says:

    Axel

    Well done.

  211. 211
    Silver Asiatic says:

    Over the past 10 years in discussions on ID, I’ve developed a certain opinion about evolutionists who post on blogs like this.

    AVS

    Hahahaha woww.
    Someone is bitter.
    Who pooped in your cheerios, Silver?

    Not bitter at all, AVS. Comments like yours make me feel all warm and fuzzy.

  212. 212
    Silver Asiatic says:

    Dionisio @ 222.

    That’s right. As I tried to explain to DNA_Jock, the simple task of describing what is observed is a major challenge for biologists in the cases you cited. They don’t even know how these things function.

    The claim that they know the evolutionary origin of these same things? It’s laughable. Even though the task of interpreting findings in an evolutionary framework is ridiculously easy (“these features could have evolved from an ancestor that might have existed”), there’s little interest in that kind of storytelling and as you mention, there’s too much information to deal with.

    I think your steady effort just to post summaries or conclusions of recent papers, highlighting the incredible complexity and tentative understanding of what is found says a lot more than many heated arguments can say.

    Evolutionists, apparently, can look at molecular fine-tuning and tell themselves that the Darwinian fairytale is untouched.

  213. 213
    Dionisio says:

    #230 Silver Asiatic

    You’ve made interesting observations. Thank you.

    The most exciting part of the ongoing research is not what remains unknown, but what is known and what will be known, because it sheds light on elaborate cellular and molecular choreographies that are orchestrated within the biological systems. That’s why we look forward, with so much anticipation, to reading future papers written by seriously dedicated researchers.

  214. 214
    Dionisio says:

    #229 Silver Asiatic

    The interlocutors who keep writing personal attacks, calling us names, using foul language, whining about our writing styles, complaining about our highlighted text, barking up the wrong trees, they appear to be the bitter ones. They seem to intentionally avoid any serious discussion on the real subjects, though sometimes they appear to be serious.
    Did they have only vinegar for breakfast after they got up in the morning? Is there another explanation for their bitter attitude?

  215. 215
    AVS says:

    Since you guys are so sure it’s a “plain fact,” why not link me to a paper that has one of these “lies and/or delusions.”
    I’m just interested in an example so that I can see you side.

  216. 216
    Dionisio says:

    #225 DNA_Jock

    Post #209 and the posts referenced from 209 will help other readers in this blog to see how AVS (who provoked this senseless debate), have avoided answering relatively easy questions, directly associated with his own initial provocation.
    You and all your party comrades act the same way and have avoided answering simple questions. Your posts in this blog are sufficient evidence of your attitude problem and provide a clear hint of your real motives in this blog: mocking and making personal attacks.
    Review the posts indicated by #209 before you whine more.
    Also the posts referenced in #187 and #190 could help you to recover your short-term memory.

  217. 217
    Dionisio says:

    #233 AVS

    The same ‘bitter’ medicine prescribed to your buddy in post #234 applies to you too.
    Complete your ‘homework’ before coming back to complain more.
    Also the posts referenced in #187 and #190 could help you to recover your short-term memory.

  218. 218
    Silver Asiatic says:

    AVS @ 233

    To do no more research than it’s worth, I just went back a couple of weeks on news posts here on UD. If you want to go back and read some more delusions, try the Evolutionary Psychology links that are plentiful here.

    Lies:
    http://www.newscientist.com/ar.....MFb2C6TKxw

    Delusion (you can find the paper):
    http://www.uncommondescent.com...../#comments

    Lies
    http://retractionwatch.com/201.....etraction/

    Lies:
    “Does anyone remember Richard Dawkins in the New York Times mocking Mike Behe’s Edge of Evolution …By referencing human dog breeding? I do. Well … Here. It was appalling, the way Manhattan sophisticates so easily swallowed something that was so obviously untrue. First, Dawkins demanded that we not pay any attention to the fact that dog breeding is a form of design …”

    Lies:
    http://www.uncommondescent.com.....e-as-well/
    Life certainly looks designed. Design language unintentionally pervades mainstream papers despite a bias against intelligent design. It’s so noticeable that articles have been written urging scientists to avoid teleological language (that is to say, design language) and use more evolutionary language. In other words, more spin.

    Delusion
    http://www.uncommondescent.com.....ke-people/

    Delusion
    Despite our intuition that humans are a species distinct from other animals, attempts to define what makes us unique continue to confound.
    http://www.uncommondescent.com.....ke-search/

    Lie/Delusion
    http://www.uncommondescent.com.....an-speech/
    The finding could help answer a big question about our human ancestors’ ability to produce speech before they developed a modern vocal tract and brain. If orangutans and other great apes can make speechlike sounds, it stands to reason that early humans could too, Shumaker says.

    Lie/Delusion
    http://www.uncommondescent.com.....chers-say/
    “Our findings suggest that stone tools weren’t just a product of human evolution, but actually drove it as well, creating the evolutionary advantage necessary for the development of modern human communication and teaching,” said Thomas Morgan, lead author of the study and a postdoctoral researcher in psychology at UC Berkeley.

    Lies
    http://www.uncommondescent.com.....uge-fraud/
    “Anthropology is going to have to completely revise its picture of modern man between 40,000 and 10,000 years ago,” said Thomas Terberger, the archaeologist who discovered the hoax. “Prof Protsch’s work appeared to prove that anatomically modern humans and Neanderthals had co-existed, and perhaps even had children together. This now appears to be rubbish.”

  219. 219
    Radioaction says:

    Silver, I think they were looking for scientific papers where phrases such as “might have evolved, may have emerged, or could have emerged” could be found. Not a bunch of 2nd or third-hand links.
    But that’s just my opinion.
    I mean it sounded like you guys were so sure of yourselves with all the “plain fact” talk.
    I’d be interested in reading a published paper with one of those phrases in it that wasn’t in any way supported.
    From my experiences, I have not known any scientists to publish claims without supporting them with evidence.

  220. 220
    Silver Asiatic says:

    Radioaction

    Silver, I think they were looking for scientific papers where phrases such as “might have evolved, may have emerged, or could have emerged” could be found.

    Go to Google Scholar. Type “might have evolved” in the search box. See what you find.

    Not a bunch of 2nd or third-hand links.

    Did you read them? They point to scientists who have published papers. What you do then is use a search engine to find the paper.

    But that’s just my opinion.

    You’re certainly entitled to your opinion, as I am mine I’d hope.

    I mean it sounded like you guys were so sure of yourselves with all the “plain fact” talk.

    Could you show me where I used that phrase? It should be pretty simple – you just need to search this thread and not even have to use google. Failing that, you’re looking for documented evidence? I’m afraid that if you can’t reference what I said correctly on a very brief thread, you won’t be able to determine the quality of speculative statements like “could have evolved” in scientific papers.
    On that …

    I’d be interested in reading a published paper with one of those phrases in it that wasn’t in any way supported.

    Show me your interested by posting some summaries where the phrases are used. Then tell me how you determined the precise strength of the evidence given to support the “might have evolved” conclusion.

    From my experiences, I have not known any scientists to publish claims without supporting them with evidence.

    It’s possible that you have very little experience with these evolutionary claims, so that would be understandable.

    Again, show me how you determine the precise strength or weakness of evidence given to support the “might have” or “could have” evolved conclusion.

  221. 221
    DNA_Jock says:

    AVS (@233) was responding to Axel (@224)

    It’s a plain fact, they build up a wonderful edifice of completely gratuitous speculations…. until you backtrack and arrive at the first ‘artistic’ postulation… and then go forward again, pondering each step of the way.

    Hence Radioaction’s use of the collective phrase “you guys”.
    Hey, at least he didn’t refer to you as a “fellow traveller” (ggg).

    I reviewed your links marked “Lies”, Silver, and I found that all the lying was being done by the IDists.

    On the other hand, I was rather surprised that you revealed ID’s top secret research technique:

    Go to Google Scholar. Type “might have evolved” in the search box.

    Dionisio has made a career out of the “is unknown” search.

    Do any of “you guys” actually bother to read the papers you cite?

  222. 222
    Dionisio says:

    #237 Radioaction

    From my experiences, I have not known any scientists to publish claims without supporting them with evidence.

    Really? But what kind of evidence? Verifiable?

    Ever heard of peer-reviewed papers retracted?

    Even recently? They are publicly known.

    Obviously, the majority of researchers are not into that fraud thing.

    🙂

  223. 223
    Axel says:

    Dio,

    De nada, amigo.

  224. 224
    Axel says:

    Evidence relating to ‘out of body experiences’, and hence mind/body dualism is conclusive, so, if none of them have the gumption to look for a place to start, that should serve admirably.

    Of course, the narrow confines of scientism make the whole enterprise a joke, a priori, and very poor one at that.

  225. 225
    Dionisio says:

    #239 DNA_Jock

    Are you trying to write funny or sarcastic comments?

    Your comments should have been posted before my #231 for your empty arguments to at least ‘appear’ more intriguing.

    But anyone who read my comments to Silver @231 could find your post @239 intentionally misleading. What else is new?

    BTW, I’ve written several times before -in other threads- the same idea expressed in #231, just with slightly different wording.

    It’s a different thing to ask questions about a text one may not understand yet. Or to highlight any part of a text that one may not understand well or that may require more careful reading later, in order to clarify some related details.

    PS. Don’t forget your homework assignment in post #234. Was your post #239 in reaction to my #234? Yuk! Is that the best you can do? Poor thing.

  226. 226
    Radioaction says:

    Alright, went to google scholar, as you said. Over 1 million hits. Many of them have the phrase or a version of it in the title of the paper, and the author(s) subsequently explain the evidence behind their claims within the paper. Papers with these phrases within the text also provided evidence of their claims by either directly giving the evidence or citing specific papers that provide the evidence.

    I did not read the links because what you were asked for was a single specific paper that uses one of those phrases and does not support it with evidence. I cannot find those phrases in any of your provided links. As for fraud in science, you will find it in small amounts in every field of research unfortunately. Do you think Intelligent Design research is immune to this?

    Everyone is entitled to their own opinion, but supplementing opinion with evidence certainly adds more weight to said opinion.

    There’s no need to be uncivil, I was simply lumping you and Axel together, since you both sounded so sure of yourselves. As I said, I would be interested in reading a paper that makes such claims without evidence, particularly one within cellular biology. Feel free to produce one if you are as sure of yourself as you appear.

    Here are some examples of papers that use phrases you don’t like, and also back them up with evidence:

    Biologic insights from structures of two-component proteins. 2009. Gao & Stock.
    In this paper they use the phrase “might have evolved,” twice. Both times they back the claim with a comparison among a number of phosphatase and kinase proteins and cite a paper that also supports their claims.

    Molecular dynamics simulations of biomolecules. 2002. Karplus & McCammon.
    In this paper they talk about how “there may be evolutionary selection for dynamics” in protein function. They back this claim in a section about the dynamics of acetylcholinesterase and its function.

    Structural symmetry and protein function. 2000. Goodsell & Olson.
    In this paper they make the claim that a specific interleukin “may have evolved” in a certain manner and they talk about the evidence behind this as well as citing the specific paper that some of these concepts originated from.

    I don’t determine “precisely” how strong or weak the evidence is behind these claims; it is a matter of reading the evidence and thinking about it. Does it make sense? Does it agree with what is known? Do any cited references further the claims?

    Do you know of a better way to determine the quality of an argument?

    Sure, it is possible that I have little experience, although I have presented scientific papers above that both, make the claims we have been talking about and support them with evidence. I’m still waiting on a single paper from you. I honestly wouldn’t be surprised if they are out there, there is a wide spectrum of researchers, some good, some not so much. I just thought you had a paper or two in mind when you originally spoke about these phrases with such certainty.

  227. 227
    Silver Asiatic says:

    Radioaction

    Alright, went to google scholar, as you said. Over 1 million hits. Many of them have the phrase or a version of it in the title of the paper, and the author(s) subsequently explain the evidence behind their claims within the paper.

    First of all, I commend you for actually pursuing my suggestion and doing this research. You’ve noted those examples (and “could have evolved” is another one giving a million plus hits).

    I’ll mention below, “might have evolved” is ambiguous. What about “might not have evolved”? These are subjective interpretations and as you state, you have no means to weigh them for strength or weakness.

    Papers with these phrases within the text also provided evidence of their claims by either directly giving the evidence or citing specific papers that provide the evidence.

    There’s no direct evidence that any of those things evolved. It’s speculative. It’s based on assumptions which are also unobserved (common descent).

    I did not read the links because what you were asked for was a single specific paper that uses one of those phrases and does not support it with evidence.

    I wasn’t asked that. So again, should I question your ability to evaluate what is written. Can you evaluate the quality of evolutionary speculations? Can you accurately evaluate the strength or weakness of evidence in this regard?

    I cannot find those phrases in any of your provided links.

    From the scientist in the second link I posted:

    In a 2008 issue of Scientific American Mind the writer Chip Walter argued, citing British zoologist Desmond Morris, that kissing may have originated from the primate behavior of pre-chewing food and passing it to the kids.

    If you’re not willing to understand that ‘may have originated’ is the same in biology as ‘might have evolved’ then we won’t be able to continue.

    Now that I showed you what you claimed didn’t exist, you could try to tell me how strong the evidence is that kissing ‘may have originated’ in the ancient past through that practice.

    As for fraud in science, you will find it in small amounts in every field of research unfortunately.

    There is fraud in evolutionary biology, yes. But more than that, there is a bias against intelligent design as indicated in one of the links I provided. There is also a systemic attempt at manipulation by use of language.

    There’s no need to be uncivil, I was simply lumping you and Axel together, since you both sounded so sure of yourselves.

    I’d call a failure to admit a mistake as a form of uncivility, myself. You made a mistake.

    Biologic insights from structures of two-component proteins. 2009. Gao & Stock.
    In this paper they use the phrase “might have evolved,” twice. Both times they back the claim with a comparison among a number of phosphatase and kinase proteins and cite a paper that also supports their claims.

    From that paper:

    “Certainly, HKs might have evolved diverse strategies optimized for individual systems to regulate kinase/phosphatase activities. ”

    You, apparently, think there is evidence supporting this. You cannot give the precise strength or weakness of the evidence, that much is known.

    But most importantly: What is a ‘strategy’ in this case? You’re claiming there’s evidence that a “strategy” evolved. Again, what is a “strategy”?
    Then beyond that, what is an “optimized strategy”?
    What does “optimized” mean and how did evolution do it? What evidence is there that this happened — admitting you have zero direct evidence?

    Molecular dynamics simulations of biomolecules. 2002. Karplus & McCammon.
    In this paper they talk about how “there may be evolutionary selection for dynamics” in protein function. They back this claim in a section about the dynamics of acetylcholinesterase and its function.

    “There may be evolution selection” means that “there may not be evolutionary selection”.
    What is the precise likelihood that there “may not be”? On what basis can it be determined that one or the other is more or less likely?

    I don’t determine “precisely” how strong or weak the evidence is behind these claims;

    Very good. Of course you can’t. Even the researchers cannot do this. The evidence could be very weak. The evidence could be based on the assumption that ‘similarity means ancestry’, which is a standard evolutionary assumption – which could be entirely false (and is false in cases of convergent evolution).

    So, with no means of weighing the evidence, the evidence may in fact be zero. Speculations on zero evidence, without admitting that it “may not have evolved” is what I call a delusion or lie. You’ve exposed several case of that already,

    it is a matter of reading the evidence and thinking about it. Does it make sense? Does it agree with what is known? Do any cited references further the claims?

    This is a subjective interpretation of data. It can render evidence meaningless. It can claim not to actually see evidence, or claim evidence is so weak as to not exist. It can claim that evidence is very strong, based on personal interpretation.

    When we’re talking personal, subjective interpretation – here’s where bias, lies and fraud play a part.

    Do you know of a better way to determine the quality of an argument?

    Yes, show me the observed evidence. Repeat it in a lab. Demonstrate that “this evolved from that”. Don’t use personal bias to claim “might have evolved” when it could be more likely that it “did not evolve”. Would you say, two apples plus Two apples “might equal four apples”?

    I’m still waiting on a single paper from you. I honestly wouldn’t be surprised if they are out there, there is a wide spectrum of researchers, some good, some not so much. I just thought you had a paper or two in mind when you originally spoke about these phrases with such certainty.

    You showed me papers that gave zero direct evidence that anything evolved.
    You then said you couldn’t tell precisely how strong or weak the evidence that you found in the papers actually was.

    If I say the evidence is so weak that it does not exist, you have no real basis to counter that.

  228. 228
    Silver Asiatic says:

    Axel

    Evidence relating to ‘out of body experiences’, and hence mind/body dualism is conclusive, so, if none of them have the gumption to look for a place to start, that should serve admirably.

    Fascinating point regarding evidence.

  229. 229
    Axel says:

    Yes, indeed, oh wily Silver Fox, considering that the monitoring equipment the patients were hooked up to, would have been as sophisticated as one might expect, and others, leading-edge. Plus they were subject to more rudimentary procedures such as the fitting of blindfolds and ear plugs.

    I watch those videos a lot. Absolutely fascinating, particularly the pitch of the emotional body language, and the sometimes wry humour.

    That’s the weird thing, though. They seem unable to distinguish between gratuitous, open-ended speculation, conjecture, work-a-day evidence for practical purposes, and conclusive evidence.

    They remind me of John Steinbeck’s words:

    “Socialism never took root in America because the poor see themselves not as an exploited proletariat but as temporarily embarrassed millionaires.”

    Rationality, in the here and now, never took root among atheists, because they see themselves, not as insanely deluded numpties, but as temporarily- unrecognised geniuses, just waiting for their promissory notes to become cashable.

  230. 230
    Axel says:

    ‘“There may be evolution selection” means that “there may not be evolutionary selection”.
    What is the precise likelihood that there “may not be”? On what basis can it be determined that one or the other is more or less likely?’

    ROFL. Silver Fox , you’re a cruel *******! And you just get meaner ‘n’ meaner!

  231. 231
    Radioaction says:

    No. “Might have evolved,” and every variation of this statement is not ambiguous. These statements are made in published research when there is evidence to back it up. There can be evidence that one protein may have evolved from another protein, just as there can be evidence that one protein did not evolve from another protein. “Might have evolved” and “unlikely to have evolved” (or some variation) would be used in these cases respectively. These statements are not subjective because to my knowledge, each time claims like these are made in published research, evidential support is provided.

    What I said was “I don’t determine precisely how strong or weak the evidence is.”

    “Precisely” is the key word. I can judge the strength of an argument just fine, but there is not an objective way to “precisely” measure how strong an argument is. The question is, does the argument convince you? Obviously you, along with many of your friends here, require an inordinate amount of evidence to be convinced of anything that disagrees with your personal beliefs. The only “direct evidence” you guys would be willing to accept is a stepwise walkthrough of every tiny step in evolution and until provided with this, you convince yourself that the entire field of evolutionary biology is nothing but a pile of “lies/delusions.” This is despite the massive body of work in the field of evolutionary biology, along with the evidence from every other field of biology that supports it. You choose to ignore all this because of a few examples of fraud (the UD favorite of which is over 100 years old). As I said, you will find fraud in every field or research. I note that you did not answer my question about whether or not you think design research is immune to this. I’ll give you a hint: it’s not.

    You were asked exactly that. Earlier you were asked for “a paper that has one of these lies and/or delusions.” We are still waiting for said paper. It would be great if the subject of the paper was on some form of cellular biology if you can manage it.

    Whether there is a bias or not against intelligent design doesn’t matter. There is bias against anything that shifts paradigms in science. If a new finding or idea really is better than what’s currently accepted, it will eventually find its way to the table. Just look at the original opposition to the chemiosmotic model. Intelligent design has had a while to make their case, and have failed time and time again. They have their own little research institute, researchers, and funding; surely if they had something of substance we would have seen it by now, no?

    I did not make a mistake, don’t worry. “You guys ” included you and axel, the same as AVS said earlier.

    DNAJock didn’t seem to have any issue understanding this. Maybe it’s your ability to evaluate what’s written that we should be worried about.

    There is evidence supporting all of the claims I cited from the papers. I briefly mentioned this evidence and how it was presented. Feel free to read about it for yourself and decide its strength. Your problem is that “Evolutionary interpretations get less weight (from me) than mere facts about observations.” Do interpretations of data in cellular biology get less weight from you as well? How about any other field of science, for that matter. They are all based on interpretation of data and it is up to the reader to decide on their validity. You, I will assume, decide that evolutionary interpretations are invalid simply because it disagrees with your personal belief system. The requirements for evidence-based claims are just as strict in evolutionary biology as they are in cellular biology and any other scientific field.

    “Yes, show me the observed evidence. Repeat it in a lab. Demonstrate that this evolved from that.” Open an evolutionary biology book, open a journal dedicated to evolutionary research, it’s all there, you just choose to get your information on evolution from websites like UD.

    “If I say the evidence is so weak that it does not exist, you have no real basis to counter that.”

    I can show you the paper (as I have), tell you about the evidence in the paper that supports the claims (as I have), point you in the direction of other literature that supports these claims (as I have), and your response is that the evidence does not exist. That’s your choice.

    The bottom line is this: We are light years beyond Darwin’s original idea. The basics he outlined still hold true and are the basis of the theory of evolution, but since his publications the theory itself has evolved based on the vast amount of information coming out of every field in biology. You can be skeptical all you want of specific claims that one protein “might have evolved” from another protein, but to believe that every scientist who makes these claims is lying/delusional or that the entire field of evolutionary biology is made up of lies/delusions?

    Now that’s delusional.

  232. 232
    DNA_Jock says:

    Dionisio,

    You keep referring me back to your post #209, and “the posts referenced therein”. But post 209 reads

    #205 AVS

    First read carefully post # 204 and then come back with more questions.

    BTW, are you also a paid cover agent working for the admin of this site, pretending to be stubbornly unpleasant, so that the discussions turn senseless, but heated enough to attract the attention of trashy talk show audiences, thus increasing the site traffic?

    Or you do all that voluntarily?

    Is your constant foul language included in your contract?

    Or is it part of your party line?

    204 (which is likewise addressed to AVS) references some of your earlier posts, which I had responded to @198.

    Frankly, you’re getting quite incoherent.

  233. 233
    Dionisio says:

    #250 DNA_Jock

    You’re wrong again. You think that you have responded, but you have not.

    Try again, if you really want to. After all, deep inside, you may not be interested in responding my questions. At least that’s the perception one gets after reading your posts.

    It’s up to you, but definitely you have not responded. Whatever you think you responded may not qualify as a serious response.

    However, you’re not obligated to respond. You know that.

    Think about it.

    BTW, the post #s directly or indirectly referenced in my posts are valid for AVS and for you.

  234. 234
    Silver Asiatic says:

    Radioaction 249

    That was a long reply. I always keep in mind that, given the overwhelming support in the biological community for modern Darwinian theory, that evolutionists (like yourself) on this blog should not be defending the theory against ID, which according to you, has nothing substantive to offer.

    Instead of defending, you should (I think) try to promote evolution among skeptics like myself. Otherwise, why bother to post on a site devoted to a ‘substanceless’ idea like ID?

    So, in all of that response, I notice quite clearly what you avoided. It’s this – and I even said “most importantly”:

    But most importantly: What is a ‘strategy’ in this case? You’re claiming there’s evidence that a “strategy” evolved. Again, what is a “strategy”?
    Then beyond that, what is an “optimized strategy”?
    What does “optimized” mean and how did evolution do it? What evidence is there that this happened — admitting you have zero direct evidence?

    Lots of questions and issues which you skipped entirely. This is merely from one paper. You’re claiming evidence supports that ‘optimized strategies’ might have evolved. But even on the theoretical level there are lots of problems with this.

    Yes, I think that evolutionary claims like that are delusional. It’s a delusion because there’s an unwillingness to explore the underlying meaning of what is said. There’s an unwillingness to ask ‘why’ evolution does the things that is claimed for it. Why does evolution create regulartory systems. What does a ‘strategy’ in cell function mean and how and why, precisely, did evolution create a strategy?

    Biologists don’t ask these questions. They run ahead simply on unquestioned assumptions.

    Some biologists have noted recently that ID plays an important role at least as a critical voice against evolutionary claims.

    In closing, I think you’ve fair-minded about the issue. I understand your bias – you’re defending a theory you believe in. I think that blinds you to some very serious problems with the theory, but you’re not as hardened in your position as many others we encounter. For that, again, I commend you.

    And with that, I apologize for a harsh tone in some of what I said. Years of battling with people who are quick to ridicule ID and are very quick with personal insults have shaped my attitude for the worse, unfortunately.

  235. 235
    Silver Asiatic says:

    Axel

    ROFL. Silver Fox , you’re a cruel *******! And you just get meaner ‘n’ meaner!

    I smiled at your comment (thank you!), but I hope its the strength of the argument that is getting meaner and not my personal disposition. 🙂

  236. 236
    Silver Asiatic says:

    Axel

    Rationality, in the here and now, never took root among atheists, because they see themselves, not as insanely deluded numpties, but as temporarily- unrecognised geniuses, just waiting for their promissory notes to become cashable.

    Another great point. Rationality leads to some uncomfortable truths, whereas the belief that one is a genius who stands above and beyond the rest of humanity can’t afford to be challenged by such things.

    Yes, they’re waiting for their promissory notes – excellent. Every bit of new data is filtered and adapted to support their investment.

    I guess delusional is not the right word for many – it’s actually euphemistic. If there’s an inner, conscious decision and commitment to a belief system, then it shouldn’t be excused as merely a mistaken understanding.

    At the same time, not all are liars.

    I guess its fair to say some are delusional, some are lying, some are open to correction and some are willfully mistaken.

  237. 237
    Axel says:

    We might be able to help those with some intellectual integrity.

    It occurred to me yesterday, when you commended me for pointing out that mind/body dualism had been CONCLUSIVELY proven, that maybe some of you boffins should keep a ‘running’ log on this site of what has now been EMPIRICALLY established, CONCLUSIVELY, but which the atheists’ religious beliefs will not countenance, a priori; fearful of ‘letting God’s foot in the door’.

    You could keep one log for positive, empirically-proven findings, simply proving them completely wrong, and another log for their empirically DISPROVEN findings – although the latter I suppose could not fit into all the pages of all the books in the Library of Congress. But might not the first ‘have legs’? What do you think? Don’t consider my feelings. I’ve the hide of a rhinoceros.

    I seem to remember seeing a similar compilation by Cornelius Hunter, exposing the glaring obstacles to a sound belief in evolution.

  238. 238
    Radioaction says:

    Why shouldn’t I defend it when it comes under fire?

    Especially from people that don’t know what they are talking about.

    Promoting evolution among the skeptics here is pointless; there is nothing that will change your minds.

    You know, things like “all evolutionists are liars/delusional.”

    I just like to argue and talk about biology.

    The “strategy” in this case is the way in which each histidine kinase is regulated. They state that evolution has come up with diverse mechanisms of regulation of HKs and give a couple examples that are very different. Each regulatory system is optimized for that specific system through the course of evolution; basically evolution is constantly fine-tuning selected new functions. Direct evidence is given when they talk about HK853 which has one form of activity that relies on the interface between two domains. This activity can be altered by mutations at this interface and results in a change in the reaction catalyzed by the enzyme. This is direct evidence that mutations can alter the regulation “strategy” of these proteins and that each strategy is likely to be unique and optimized for each protein and its function, over the course of evolution as shown by the two examples given.

    Anything I skipped is right there in the papers and what I have already said.

    I fear that you simply do not understand how research works. It’s not that there is an unwillingness to explore, to ask why, or what. “Run ahead on unquestioned assumptions” couldn’t be further from the truth. Biologists take tiny incremental steps to figure out the answer to a very specific question and then relate their findings to the existing body of knowledge. Publications on cellular biology focus on their main question and often relate it to evolutionary findings as in the examples I have given. It is the evolutionary biologists that focus on evolutionary questions and publications in that field focus much more heavily on providing the direct evidence you choose to ignore.

    Criticism of evolutionary claims from the ID community is of little importance. The majority of the ID community have no clue what they are talking about, as shown on PaV’s latest posted which I commented on.
    It is also redundant. There is plenty of criticism within evolutionary biology, along with every other field, as researchers continually disagree on interpretations of evidence and validity. What isn’t criticized in any of these fields is the mention of evolutionary ideas as in the paper I have cited. This is because there is no uncertainty within these fields as to whether or not evolution has occurred.

    There are no serious problems with the theory, save for the fact that we understand only a fraction of the evolutionary process.

  239. 239
    Silver Asiatic says:

    DNA_Jock 216

    You claimed that I was arguing against a ‘fictional adversary’ and wanted some references. The following article by evolutionary biologist, James Shapiro offers some insights that might help:

    http://www.huffingtonpost.com/.....25133.html

    — Richard Dawkins began his lecture by saying, “I will not only explain that Darwin had the right answer, but I will show that he had the only possible right answer.”

    — conventional evolutionists make absolutist statements like “all the facts are on my side.”

  240. 240
    Silver Asiatic says:

    Radioaction

    Why shouldn’t I defend it when it comes under fire?

    When you defend something from a non-existent threat, I recognize something in your motivation. If I defend my house against non-existent beings (predatory unicorns) it says something about me. If I spend time going to blogs about topics I think are unsubstantial (wizards who make magic potions) – then that says more about me than the topic.

    Especially from people that don’t know what they are talking about.

    There’s no threat to your theory from people who are ignorant of it.

    Promoting evolution among the skeptics here is pointless; there is nothing that will change your minds.

    I would guess that you don’t really believe that. But anyway, it would make your time spent here seem more futile and wasted. Spending time on a blog that nobody cares about, among people who are ignorant and incapable of changing their minds … it certainly makes me wonder about you.

    You know, things like “all evolutionists are liars/delusional.”

    No, I don’t know that. Please show me where you can find that quoted text.

    The “strategy” in this case is the way in which each histidine kinase is regulated. They state that evolution has come up with diverse mechanisms of regulation of HKs and give a couple examples that are very different.

    I wouldn’t call that a very precise definition of a strategy. They also do not state that “evolution has come up” with these mechanisms. You’re misrepresenting the paper. That’s been the topic under discussion.

    Each regulatory system is optimized for that specific system through the course of evolution;

    That’s an undemonstrated assertion. You’re missing a very signficant point also – evolution does not ‘optimize’ anything. Optimization refers to a value which is invisbile to evolution. If there are optimizations, then evolution works towards ‘what is better’ and is therefore directional.

    basically evolution is constantly fine-tuning selected new functions.

    You might want to read the link I offered from Ann Gauger. You’re using teleological language to describe evolution. “Fine-tuning” is something that can only be measured against a reference point. It’s also a perfect example of design language. Mutatation, selection, drift and whatever other unintelligent mechanisms you have cannot ‘fine-tune’ things. Again, that’s teleological language of directed evolution.

    Direct evidence is given when they talk about HK853 which has one form of activity that relies on the interface between two domains. This activity can be altered by mutations at this interface and results in a change in the reaction catalyzed by the enzyme.

    No direct evidence of evolution is given. Mutations ‘can’ supposedly do things. But what ‘did’ they do?

    It is the evolutionary biologists that focus on evolutionary questions and publications in that field focus much more heavily on providing the direct evidence you choose to ignore.

    As I said, there is zero direct evidence that those mechanisms evolved at all. Direct, observed evidence is watching in a lab as one thing evolves from another. You have none of that in this case.

    There are no serious problems with the theory, save for the fact that we understand only a fraction of the evolutionary process.

    I’ll ignore the contradiction in that sentence and point you to the thread on Susan Mazur’s book on UD’s front page.

    In any case, you’re totally convinced by evolutionary theory and are willing to claim that ‘there are no serious problems with it’.

    I can point out, simply, that the theory cannot even define or explain what the mechanisms of evolutionary change are or to what degree they function in nature. To that extent, it’s not a theory. A theory cannot say ‘there might be mechanisms that caused XYZ to evolve’. It has to say precisely what those mechanisms are and how they caused something to evolve. The mutation/selection notion is becoming more discredited.

    Again, see the ‘third way of evolution’ threads and/or the one I just referenced.

  241. 241
    Radioaction says:

    Silver, as I said, I enjoy talking about biology and I enjoy arguing. I don’t really care what you think about me.

    You are correct, there is no threat to the theory and time spent here by everyone is futile and wasted.

    Silver Asiatic:

    “First of all, I don’t give credence to any and all authors statements. I wouldn’t be surprised if they’re lying or delusional – I expect that from the evolutionary biology community.”

    “Statements that include conditional or speculative phrases like “might have evolved” or “may have emerged” or “could have developed” I usually consider to be lies and/or delusions. And that’s what most of evolutionary science is, in my opinion.”

    Apparently you forgot?

    It’s not “a very precise definition of strategy?” Move the goalposts much?

    They are making the claim that evolution produced these varying regulation strategies seen in different histidine kinases. I am not misrepresenting the paper, just saying it in words I was hoping you’d understand.

    Evolution doesn’t optimize? Are you kidding me? Evolution certainly does optimize and fine-tune. Just take a look at the fin-tuning of organisms to their environment. Whether it’s teleological language or not, it is a description of what happens over the course of evolution. Once again the ID argument relies on word-play.

    No it’s not that mutations “can supposedly” do things. Certain mutations DO these things. You’re requirement that science figure out exactly how “one thing evolves from another” by recreating evolution in a lab, is childish.

    There was no contradiction. We may not entirely understand how evolution works, but it is quite obvious that it is occurring. If you’re going to make statements like “evolution isn’t a theory,” then this conversation certainly is futile and a waste.

    Good day.

  242. 242
    DNA_Jock says:

    To rebut my contention that he is arguing with a fictional adversary, Silver Asiatic @257 offers up the following:

    DNA_Jock 216

    You claimed that I was arguing against a ‘fictional adversary’ and wanted some references. The following article by evolutionary biologist, James Shapiro offers some insights that might help:

    http://www.huffingtonpost.com/…..25133.html

    – Richard Dawkins began his lecture by saying, “I will not only explain that Darwin had the right answer, but I will show that he had the only possible right answer.”

    – conventional evolutionists make absolutist statements like “all the facts are on my side.”

    Couple of problems here.

    I cannot find any support for Shapiro’s claim that Dawkins said any such thing, although it does sound like the kind of thing that he would say, if he as trying to get an audience’s attention…

    Anyway, Dawkins isn’t a researcher, so quoting him with attribution (were you able to) still wouldn’t meet my request @216.

    The “facts are all on my side” quote is Shapiro quote-mining Coyne. Shapiro is in fact whining about the beat-down Coyne gave him for some rather silly statements Shapiro made, such as

    The second problem is that Darwin understood only “numerous, successive, slight modifications” as the sources of inherited change. His neo-Darwinian followers have modified this position to assert that all mutations occur randomly. They insist there is no biological input into the change process. For them, the genome determines organism characteristics. They think of it as a read-only memory (ROM), which only changes by accident.

    and

    Three remarkable things about somatic hypermutation and CSR are explicitly excluded from the prevailing philosophy of genetic change. First, they are adaptive and purposeful genome changes. Second, they are functionally targeted. Third, for CSR, targeting involves intercellular signals that depend on how other cells in the immune system perceive a particular infection.

    claiming that somatic hypermutation is somehow anti-Darwinian.
    So when, in this context, Coyne says, “the facts are all on my side”, he is stating a simple fact, not making an “absolutist statement”, which would look more like this:

    …the real version of evolutionary theory – the one that has no weaknesses and which offers precise and accurate predictions with each new finding in the data.

    Also, if you believe Shapiro when he makes these uncorroborated claims about what Dawkins said, do you also believe him when he writes, in the Huffpo article you linked to,

    5. The newly discovered processes of genome change do indeed have the potential to generate “irreducibly complex” new functions. Such complex evolutionary inventions are at the center of the Intelligent Design critique of neo-Darwinian explanations, which are based exclusively on random genetic accidents and natural selection. Doubling the whole genome, distributing copies of mobile elements to different sites, and incorporating similar domains in different proteins provide the necessary raw materials for generating complex interactive networks in cells.

    I would be quite interested in trying to understand what triggers skepticism in you, although I think I already know the answer…

    But my original point remains. You were arguing with ME, and you repeatedly attributed to me views that I do not hold. Not that I’m surprised, it’s par for the course here.

  243. 243
    Dionisio says:

    DNA_Jock

    FYI – in case you didn’t notice it, as I wrote in my post #251, your post #250 failed to respond my previous posts, including my post #243.

    Did you run out of arguments?

  244. 244
    Dionisio says:

    Radioaction

    Did you see my post #240 in reference to your post #237?

    Don’t you have anything to comment on that?

  245. 245
    Dionisio says:

    AVS, DNA_Jock, and your party comrades:

    Please, note that there’s more of the same bitter medicine, enough to treat your condition that makes you criticize how others quote and highlight text in their posts. 🙂

    Here’s the link (serve yourselves):
    http://www.uncommondescent.com.....ent-544014

    🙂

  246. 246
    DNA_Jock says:

    Dionisio writes @261

    DNA_Jock

    FYI – in case you didn’t notice it, as I wrote in my post #251, your post #250 failed to respond my previous posts, including my post #243.

    Did you run out of arguments?

    LOL.

    Your post 243 refers back to 234, which refers to 209, 187, 190.
    All answered in my 198.
    FYI, your 231 is word salad.
    The incoherence continues.

  247. 247
    Silver Asiatic says:

    DNA_Jock

    I cannot find any support for Shapiro’s claim that Dawkins said any such thing, although it does sound like the kind of thing that he would say, if he as trying to get an audience’s attention…

    But if I said that evolutionary biologist Shapiro was ‘lying to get attention’ you’d be outraged, right? 🙂 Funny how it works that way.

    Anyway, Dawkins isn’t a researcher, so quoting him with attribution (were you able to) still wouldn’t meet my request @216.

    Yes, but your request didn’t meet what I posted. If Dawkins cannot be considered part of the ‘evolutionary biology community’ as I said, then we’ve got an entirely different conversation.

    The “facts are all on my side” quote is Shapiro quote-mining Coyne. Shapiro is in fact whining about the beat-down Coyne gave him for some rather silly statements Shapiro made, such as

    Your argument is with fellow evolutionist Shapiro – not me. You’re making it clear that I can’t trust what evolutionists have to say. I guess I have to run their comments by you to get the right interpretation?

    I would be quite interested in trying to understand what triggers skepticism in you, although I think I already know the answer…

    You’ve already claimed that I shouldn’t trust what Shapiro says. I only posted a link to him because he’s an evolutionist and I know you won’t care about what IDers have to say. Shapiro merely supported what I have seen in discussion blogs for years — claims about how ‘there are no weaknesses’ in evolutionary theory are very common. I don’t need Shapiro to support that.

    Here’s one of ‘you guys’ right on this very thread:

    Radioaction
    There are no serious problems with the theory, save for the fact that we understand only a fraction of the evolutionary process.

    But my original point remains. You were arguing with ME, and you repeatedly attributed to me views that I do not hold. Not that I’m surprised, it’s par for the course here.

    You’re claiming that my views were fictional. I posted an article from Shapiro that was written for the specific purpose of putting aside notions that evolutionary theory is complete. You then claim that Shapiro wrote that for manipulative (getting attention) or vindictive (against a beat-down) motives. So, he can’t be trusted.

    I said:

    Ok, you’re denying that evolutionists (I didn’t limit it to biology researchers) claim that their theory is essentially complete and explains the origin of the entire biosphere on earth.

    That’s why Shapiro wrote the article. The quotes from Dawkins or Coyne were illustrative.

    Am I supposed to believe that evolutionary biologist Shapiro just imagined the notion that fellow-evolutionists overstate claims for their theory?

    That’s very hard to believe. You see my posts as agenda-driven but I hope you don’t ignore the bias that is evident in your own views.

  248. 248
    Dionisio says:

    #263 Aurelio Smith

    Are you implying that in your post #101 you were barking up the wrong tree?
    Are you implying that your post #101 was a regrettable knee-jerk reaction?

    Is that why you did not respond to post #115?

    http://www.uncommondescent.com.....ent-541499

    If that’s the case, maybe it’s understandable.

    🙂

  249. 249
    Dionisio says:

    #265 DNA_Jock

    Is that the best you can do? Really?

    Ran out of arguments?

    BTW, what about #264?

    🙂

  250. 250
    Dionisio says:

    OT

    Disclaimer: I’m not paid by the moderators or this site admin for luring in more commenters into any discussion thread. However, it’s kind of fun to watch how some interlocutors react to different types of comments. 🙂

  251. 251
    DNA_Jock says:

    Silver Asiatic wrote:

    But if I said that evolutionary biologist Shapiro was ‘lying to get attention’ you’d be outraged, right? Funny how it works that way.

    This has to be one of the strangest, and most revealing, things I have ever read at UD. Before I walk you through my reaction to this statement, let me eliminate the most charitable explanation: You were being sarcastic – no, given the rest of your post, that doesn’t hold water : you genuinely expect me to be ‘outraged’ by the leveling of such an accusation at a “fellow evolutionist”.

    Here’s the timeline of my reaction to your statement:

    1. Why would I be outraged? I agree that he’s exaggerating to get attention.

    2. Wait a second, “lying”, that’s a strong word to use. Do you have evidence to support your contention that he is guilty of intentional falsehood?

    3. Absent any evidence of deceit, I will give Shapiro the benefit of the doubt here.

    4. I provisionally withhold agreement with the sentiment expressed.
    My reaction doesn’t even reach “somewhat miffed”. More like ”slightly furrowed brow”. (Here’s a hypothetical statement that would outrage me. “The CDC is lying about the safety and efficacy of vaccines”. This statement costs innocent lives, if believed. See the difference?)

    Trying to comprehend the point you were trying to make, the best I can manage is that the emphasis in your statement was on the word “I”, as in “But if I (Silver Asiatic, the IDist) said that [an evolutionist] was lying, you’d be outraged, right?” as in “How dare one of them bad-mouth one of us! The cheek!”

    Here’s the very important and very revealing thing: notice how, in step 1, I gave the statement something of a free ride, because I agreed (more or less) with the sentiments expressed. Only at step 2 did “System 2” (Kahneman) kick in, and I started to analyze the statement for veracity, even though I agreed with the overall sentiment. Simply put, you Silver Asiatic never get to step two: your mindset is stuck in “evolutionists always lie, except when they say things I agree with”. Evidence be damned. Reality be damned.

    The rest of your post is an impressive demonstration of this “culture wars” mindset. You assume “evolutionists” are liars and/or delusional, and you assume that I have a similar, but reversed, mindset.
    In SA-world, an evolutionist such as DNA_Jock will always agree with other evolutionists and must think that Richard Dawkins is awesome and always right, whatever he says.

    If Dawkins cannot be considered part of the ‘evolutionary biology community’ as I said, then we’ve got an entirely different conversation

    Actually, I do NOT consider Dawkins (or PZM) to be part of the ‘evolutionary biology community’. Dawkins is a writer, PZM a blogger. I have been known to refer to that pair as “arrogant dickish atheists with megaphones” at TSZ. You should visit sometime. We do have an entirely different conversation. CRD and PZM are big figures in some sad culture war that you are waging, not part of the ‘evolutionary biology community’. I just want people to keep religion out of science education, which means I am motivated to encourage people to educate themselves about biology. CRD (when in atheist mode)and PZM are actually obstacles, not allies, to me.

    Your argument is with fellow evolutionist Shapiro – not me. You’re making it clear that I can’t trust what evolutionists have to say. I guess I have to run their comments by you to get the right interpretation?

    No, try using your own brain to assess the accuracy of statements on a case by case basis. Sometimes scientists say things that are wrong. Learn to be more skeptical of those statements that you agree with, and less quick to dismiss as lies or delusions those statements that you disagree with. Stop being so lazy and engage System 2, for crying out loud!

    . I only posted a link to [Shapiro] because he’s an evolutionist and I know you won’t care about what IDers have to say.

    Completely and utterly wrong. This is a textbook example of your Culture Wars bias. You are projecting. I am almost always interested in what IDers have to say, but I do expect them to be willing to support their claims. My discussions with gpuccio bear this out, I believe.
    When Radioaction writes

    There are no serious problems with the theory, save for the fact that we understand only a fraction of the evolutionary process.

    You think this supports your strawman

    the real version of evolutionary theory – the one that has no weaknesses and which offers precise and accurate predictions with each new finding in the data. [snip] …I might say that your version of evolutionary theory could be considered a strawman as well, especially if you’re proposing it as highly certain and irrefutable.

    It doesn’t. Note the qualifiers in Radioaction’s statement.
    You write

    You’re claiming that my views were fictional.

    No. I claim you are arguing against a fictional adversary. As evidenced by your continuing efforts to ascribe to me views that I do not hold.

    Ok, you’re denying that evolutionists (I didn’t limit it to biology researchers) claim that their theory is essentially complete and explains the origin of the entire biosphere on earth.

    But I DID limit it to biology researchers. And even the atheist culture warriors that you love to hate don’t make that claim, since it encompasses OOL.

    Am I supposed to believe that evolutionary biologist Shapiro just imagined the notion that fellow-evolutionists overstate claims for their theory?

    I am quite willing to accept that people on all sides have, on occasion, overstated their claims. You should try it out sometime. But your TGTKtM is still a fictional adversary.

    You see my posts as agenda-driven but I hope you don’t ignore the bias that is evident in your own views.

    I am on the look-out for bias in my own views. I am fortunate to have had training that is extremely helpful in this regard. You, on the other hand, may well be the poster-child for confirmation bias.

  252. 252
    Dionisio says:

    Open challenge to all:

    Does anyone dare to argue against this insightful comment?

    http://www.uncommondescent.com.....ent-544994

  253. 253
    Petrushka says:

    It’s vacuous. Does that count?

  254. 254
    Dionisio says:

    #272 Petrushka

    Why do you consider it that way? Can you elaborate?

    Thank you.

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