Uncommon Descent Serving The Intelligent Design Community

Live stream of the Nelson–Velasco debate – NOW

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
arroba Email

Debate Controversy Further to “Nelson-Velasco debate: Hold it despite opposition. Anything else is “fascism,” says prof,” here’s the live stream of the debate (presumably when it starts, at 3:00 pm EST).

By the way, in case you happen to hear, during the debate, that “Creationists will be the death of science” or some such, get this, from genetcisit Todd Wood’s blog:

I just got back from the Bryan College Undergraduate Research Conference. I’m teaching an adjunct class this semester to bio majors, and two of my students were presenting. …

[evil creationists, see?]

After the conference, the department chair took me aside and shared with me the results from the latest standardized testing of the senior biology majors. The test splits up their scores in four categories: cell, organismal, genetics, and evolution. To my absolute delight, Bryan College students scored in the 99th percentile – in the evolution category! That was their highest category too. Uh oh! Who’s been teaching them evolution? Well, that would be me. The class I’m teaching this semester is called “History of Life,” which is just a euphemism for evolutionary biology. I teach straight from Freeman and Herron’s Evolutionary Analysis, and we read Darwin’s Origin of Species during the class. The students know my position on origins, and when appropriate, I bring in creationist commentary. But for the most part, it’s straight evolutionary biology. The 99th percentile means they’re outperforming most students taught by actual evolutionists.

The fact that lots of people don’t believe that a pile of kindling is a Tree of Life, doesn’t mean they can’t answer questions about what’s in the book advocating that view.

The problem is more with what’s in the book.

Follow UD News at Twitter!

Comments
AVS (#85), Your attempts to minimize the competency of creationists in evolutionary theory are noted. You said,
And, again Paul, I would want to know how many students took the test.
And again,
The only thing that has been proven is that 8 students (which were assuming) out of who knows how many, scored well on a test that was standardized to who knows what other schools. By your thinking it would seem the likely candidates for this were other christian colleges, which doesn’t say much for being in the 99th percentile then.
Your proposal sounds a little desperate. Educational Testing Service ( https://www.ets.org/ ) is the same outfit that produces the Graduate Record Exam, which presumably you will take. To suggest that it standardizes its evolutionary biology test on creationist colleges is just ludicrous. Contrary to your prejudices, some creationists, including most of those at Bryan college, really do understand evolution. Remember, their 6 year average is 98th percentile. Paul Giem
AVS, You are missing the point that was being made, because you are behind in your understanding where the conversation currently is. You stated that
The argument was whether or not the sequence is the driving factor in folding, and as I have just explained, the sequence is the driving factor with or without the use of chaperones.
That was the proposal that Annila and Baverstock originally made (in a peer-reviewed journal) and that bornagain77 repeated. However, I believe that BA77 is now agreeing to the fact that the sequence does determine the folds that are possible, and that sequence is a necessary condition for proper folding (see #47 and #48). At this point nobody is disagreeing that protein sequence is necessary for proper folding, and you would get no argument from me if you characterized sequence as the major driving factor in protein folding. You even seemed to recognize this in #50. You have also conceded that for a subset of proteins, chaperones are necessary. As you said in #57,
I’ve already stated that to my knowledge chaperones function by providing an environment in which the protein folds more easily, still driven by its amino acid sequence.
But there is another question that you do not seem to be understanding as well. It is, what percentage of proteins require chaperone proteins in order to fold correctly in vivo? And for this purpose, it doesn't really matter whether the proteins are actively folded by the chaperones, or the chaperones merely keep the proteins from folding incorrectly or from interacting with other proteins prematurely. The important point is that the proteins need the chaperones to fold properly in vivo. And here Joe is correct according to the literature. Joe quotes an article stating that
The folding of most newly synthesized proteins in the cell requires the interaction of a variety of protein cofactors known as molecular chaperones.
That would indicate that the proportion of proteins needing chaperones to fold correctly in vivo is greater than 50%. You picked option C. I will quote option C again:
C. pretend that you can still lay down the law, in which case your opinion on this can be safely ignored.
You simply can't "lay down the law". Neither we, nor the proteins, will listen. Science is finding out what nature does, not telling nature what it must do. You sound like a college student who is full of himself. Come to think of it, since you state that "actually I will have a PhD in cell and molecular biology somewhere in the next 6 years", you probably are a college student. (Either that, or you are a graduate student on a slow track.) Some of us have more education in the relevant disciplines than you do. And you are telling us not to listen to two PhD's who got their article into the peer-reviewed literature. So even if you had a PhD, you couldn't "lay down the law". Experimental evidence and logic are the only things we are required to listen to. That is why you need to produce an article if you wish to persuade us that in fact, most proteins in vivo do not require chaperones. Your comment, "I am arguing against need for the chaperones that directly effect protein folding", is currently arguing against a straw man. Nobody here is any longer arguing that chaperones are folding proteins in the way the chaperones dictate regardless of the proteins' sequences. But if you state it in a slightly different way, "I am arguing against need for the chaperones that directly affect protein folding", then you will meet more resistance. A chaperone that keeps a protein from folding in the wrong direction is aiding in its proper folding. If it makes you feel better, you can take out the word "directly". But the chaperone in question definitely affects protein folding. Paul Giem
I know what the paper says, moron. I did not take the abstract out-of-context and you cannot show that I did. You have been unable to follow anything that I posted. It's as if you are just a mental midget cry-baby.
That abstract is referring to all subtypes of chaperones, the chaperones that directly aid folding by imparting steric information and those that don’t.
I know that. I never said that chaperones were only used to assist protein folding. The abstract says tat most proteins require chaperones to assist in folding. That refutes your ignorant claim that chaperone assistance is rare for protein folding. You are a poseur. and a liar. Joe
Joe, we've talked about all of these things. Yes context is very important, and you took that abstract out of context when you copy and pasted it as "evidence" for yourself. That abstract is referring to all subtypes of chaperones, the chaperones that directly aid folding by imparting steric information and those that don't. Bye bye little Joey, thanks for the laughs. AVS
AVS YOU don't know what you are talking abt. Yoiu are a lar and a loser.
1. There are many types 2. A small subset of these type directly aid protein foldingg
So far so good
3. Most proteins can fold on their own
Evidence please.
4. A small subset of proteins have an absolute requirement for chaperones for correct folding
Reference please. Your word means nothing here.
5. As far as I am aware, the small subset of chaperones that aid folding, function by taking in the unfolded protein and provide an environment in which the amino acid sequence can correctly fold.
LoL! As far as we are aware AVS is a liar and a moron.
It should be noted when the word “chaperone” is used, it is not only referring to the small subset of chaperones that directly aid in the folding of the protein, but also the many other types of chaperones that do not aid folding.
LoL! It all depends on the CONTEXT.
For example: “The folding of most newly synthesized proteins in the cell requires the interaction of a variety of protein cofactors known as molecular chaperones.”
Peer-review
With these facts in mind it shouldn’t be hard to see who actually knows what they are talking about.
AVS can't even follow along. He has to lie, misrepresent and bloviate. So AVS is nothing but a lying punk and cannot stand that I corrected him. Joe
I always do make sure that person doesn't know what they are talking about before I call them out on it. It usually doesn't take long to figure it out. And, again Paul, I would want to know how many students took the test. Is it a requirement for graduation, or did they just select 8 of their top students to take the test so they could hand out stats like these. The only thing that has been proven is that 8 students (which were assuming) out of who knows how many, scored well on a test that was standardized to who knows what other schools. By your thinking it would seem the likely candidates for this were other christian colleges, which doesn't say much for being in the 99th percentile then. AVS
There is no such thing as a degree in "protein folding," but actually I will have a PhD in cell and molecular biology somewhere in the next 6 years. Once again, no. You have to be careful when reading the article because when they say "function in protein folding" they don't mean the chaperone actually directs folding. IF you just read the abstract, you'll see that they say Hsp70/40 function in protein folding, and then they will go on to explain in more detail that these proteins just keep the newly synthesized protein from aggregating. Hsp60 is the only chaperone they mention which directly aids folding of the newly synthesized protein. And as I have repeatedly said, this chaperone functions by providing an environment for increased efficiency of sequence-driven folding. The argument was whether or not the sequence is the driving factor in folding, and as I have just explained, the sequence is the driving factor with or without the use of chaperones. I am not arguing against the need for chaperones as a whole, I am arguing against need for the chaperones that directly effect protein folding. And I know it to be a fact that the majority of proteins in the cell do not need chaperones to direct their folding. "It would seem that if the folding of a protein requires the interaction of various protein cofactors known as chaperones, those chaperones directly aid in the folding of that protein." Just in case I didn't make myself clear, NO. This is completely wrong and also the source of Joe confusion. the word directly is what makes this statement wrong. As I have just said, the need for chaperones that directly aid folding of a protein sequence is small in the cell. The majority of proteins use chaperones, but they do not "directly" aid folding, they merely hold the protein in its unfolded state or partially unfolded state. Joe does not have a reference that supports his position. He thinks he does, but that is only because he has no idea what he is talking about. So yes, I choose C, but my "opinion" cannot be safely ignored because I actually know what the hell I am talking about. Wiki most certainly is reference enough for post here at UD, you hold this site in much to high esteem. AVS
AVS (#64), You said,
I see Paul, obviously at least some of the students have an understanding of the basics of evolution, the numbers don’t lie. But I would suggest that you be careful about saying the “whole class” scored in the 99th percentile, as this is not what was said. What was said was that “students” scored in the 99th percentile. I would like to know if all their students took the test or was it just a select few? How many students were actually in the 99th percentile? Who else takes the test? I know my university doesn’t require biology students to take tests like this.
Thanks for your concession that at least some creationist students understand the basics of evolution. I presume that you will be cautious in the future about saying things like "You really don't understand evolution" to a creationist or ID proponent without first making sure that the person doesn't actually understand. If you look at the website, there are 8 named students. So it appears that 8 students got the 99th percentile. One may argue that these are 8 out of a huge number of students. I doubt that there are that many biology students at Bryan College. But there is another piece of information that can be gotten here (scenario 5) It says,
over the past 6 years, Bryan's Biology majors have averaged scores in the 98th percentile in their ETS Major Field Tests.
So this finding was not just a fluke. I don't know why your university doesn't require biology students to take tests like this. But I can see why Bryan College might want to do so. There would be those who would criticize them for going to a creationist school and not learning about evolution. Perhaps they wish to give the lie to such suppositions. They have more to prove than your university. It does look like they have pretty much proved it. Paul Giem
AVS (#81), Before we accept the law you are laying down, perhaps it is fair to ask who gave you the role of lawgiver. Do you have a master's or PhD in protein folding? Or are you just spouting what you were taught without any idea that science may have advanced from there? I will agree that there are many types of chaperone proteins. From my reading of Joe's reference (#79), it appears that most can function as helpers for protein folding, either by actually encouraging folding or by discouraging the aggregation that would otherwise occur, which seems to me to still be necessary for folding in vivo. So your point 2 appears to be falsified by the reference. Your point 3 is true, but misleading. If you will note, the reference points out that in vitro and in vivo are two different environments, with some folding taking seconds in cool, dilute solutions that would not apply in vivo. To quote,
However, the experimental conditions necessary to successfully fold many proteins, especially larger ones, in vitro, are very constrictive, usually requiring very low protein concentration and long incubation times and are usually unphysiological (e.g., relatively low temperatures).
If one has a protein that will not spontaneously fold in the cell at ambient temperatures without a chaperone, it is fair to say that it requires a chaperone (or chaperones) to fold properly in the cell. I noticed that you tried to sidestep the force of Joe's quote by claiming that
It should be noted when the word “chaperone” is used, it is not only referring to the small subset of chaperones that directly aid in the folding of the protein, but also the many other types of chaperones that do not aid folding. For example: “The folding of most newly synthesized proteins in the cell requires the interaction of a variety of protein cofactors known as molecular chaperones.”
I'm not sure you are listening to yourself when you say this. It would seem that if the folding of a protein requires the interaction of various protein cofactors known as chaperones, those chaperones directly aid in the folding of that protein. And according to the quote, most proteins fall into that category. Joe has a reference, peer-reviewed, supporting his position. You have three choices: A. admit you were wrong, or at least that the available evidence supports his position, B. find a newer reference supporting your position, or C. pretend that you can still lay down the law, in which case your opinion on this can be safely ignored. And for this, Wikipedia is not a reference, although if they have references to the peer-reviewed literature, those references (if you read them) might be adequate. Paul Giem
Alright, let me lay down the law for everyone since a certain individual is exhibiting the exact traits of a typical UDer; a complete misunderstanding and yet complete confidence in the bullshit that comes out of their mouth. Here are the facts about chaperones: 1. There are many types 2. A small subset of these type directly aid protein foldingg 3. Most proteins can fold on their own 4. A small subset of proteins have an absolute requirement for chaperones for correct folding 5. As far as I am aware, the small subset of chaperones that aid folding, function by taking in the unfolded protein and provide an environment in which the amino acid sequence can correctly fold. It should be noted when the word "chaperone" is used, it is not only referring to the small subset of chaperones that directly aid in the folding of the protein, but also the many other types of chaperones that do not aid folding. For example: "The folding of most newly synthesized proteins in the cell requires the interaction of a variety of protein cofactors known as molecular chaperones." With these facts in mind it shouldn't be hard to see who actually knows what they are talking about. AVS
AVS:
I’m not saying that a small subset of proteins would be able to fold correctly without chaperones.
Most proteins wouldn't be able to. And according to what YOU sed the amino acid sequence determines the fold. However the fact that chaperones are required refutes that claim.
I’m saying that all the chaperones do is guide sequence-specific folding.
Not exactly. The sequence specificity will allow the assisted folds to be held after the chaperone leaves the scene. Joe
AVS sed that chaperones assisting in protein folding is rare. I give you the following as a refutation: Chaperone Mediated Protein Folding:
Abstract The folding of most newly synthesized proteins in the cell requires the interaction of a variety of protein cofactors known as molecular chaperones.
Oops. As I already knew, I know more about biology than AVS. And without the chaperones those proteins would never fold into their required shape. AVS has never even addressed what I have been saying. Talk about mental retardation... Joe
I'm not saying that a small subset of proteins would be able to fold correctly without chaperones. I'm saying that all the chaperones do is guide sequence-specific folding. I honestly think you have some form of mental retardation...or your just a troll. Bye little Joey, take care now! AVS
At least AVS admits that he is a wall. That is a start. Again, it is a fact that without the chaperones, the proteins that need them would NOT find their functional shape. AVS doesn't even respond to what I am saying. AVS is a pure ass and a moron. Joe
Joe, how bad are you bleeding from banging your head against the wall so much? The use of chaperones for folding is rare, and I've already explained numerous times that chaperones work by catalyzing sequence-specific folding. You have absolutely no idea what you are talking about. When you have something new to say, let me know. Good day. AVS
AVS- you are full of it. Without the chaperones the polypeptides would not find their functioning shape. And according to your original claim the same amino acid sequence should produce the same protein with the same folds. It doesn't, you lose. Joe
I don't hate anybody, but when someone starts screaming their religious nonsense at passerbys, yelling about how "evolution is a lie" with absolutely no evidence for their claims, it bothers me a little. In the end everyone thinks the guy is a complete psycho, but it still bothers me that people can be so ludicrous. Anyways I realize what I'm doing on here is comparable, but at least I back up my claims with scientific facts. AVS
Dr. Geim forgive me for posting one more time, but AVS you state:
When I stop seeing your creationist nutjob friends on my campus screaming about how “Jesus loves me and….hates me” then I will stop being an ass to you guys.
So AVS, I take it you are defending atheistic/materialistic thinking for how we got here, (aka Darwinism), on UD because you hate some or all Christians on your campus? Please clarify as to whether you hate some or all of the Christians on your campus? Should I hate all or just some atheists in the world because of the deeds of Stalin and Chairman Mao?,,, But anyways, I take it that you think that you have no soul to be concerned about and that all this life after death talk is just a bunch of malarkey???? Well contrary to what you may imagine to be true for reality, the fact is that there is now empirical evidence for a 'transcendent' component to your being which is not reducible to matter and energy. In fact to hash this out just a bit more, Naturalism/Materialism predicted that we are merely our material bodies with no transcendent component to our being, and that we die when our material bodies die. Theism predicted that we have minds/souls that are transcendent of our bodies that live past the death of our material bodies. Transcendent, and ‘conserved’ (cannot be created or destroyed) ‘non-local’, beyond space-time matter-energy, quantum entanglement/information, which is not reducible to matter-energy space-time, is now found in our material bodies on a massive scale.
Quantum Information/Entanglement In DNA – short video http://www.metacafe.com/watch/5936605/ Quantum Entanglement and Information Quantum entanglement is a physical resource, like energy, associated with the peculiar nonclassical correlations that are possible between separated quantum systems. Entanglement can be measured, transformed, and purified. A pair of quantum systems in an entangled state can be used as a quantum information channel to perform computational and cryptographic tasks that are impossible for classical systems. The general study of the information-processing capabilities of quantum systems is the subject of quantum information theory. http://plato.stanford.edu/entries/qt-entangle/
In fact, not only is this non-local, beyond space and time, quantum information in the cell not reducible to (or emergent from) the energy and mass of the body as Darwinism holds, but all the energy and mass of an entire human body can ‘theoretically’ be reduced to quantum information and 'instantaneously' teleported elsewhere in the universe. A fact which is completely contrary to materialistic thinking:
Quantum Teleportation of a Human? – video https://vimeo.com/75163272
Thus AVS, while you may laugh at, scoff at, and demean, people who take the destiny of their souls seriously, the fact of the matter is that empirical science itself is now to the point of verifying their basic 'nutjob' belief to be true!!! i.e. Science itself now strongly indicates that there is indeed a transcendent 'soul' within out bodies to be concerned about. Myself, I take the 'life after death' matter seriously:
Two very different eternities revealed by physics https://uncommondesc.wpengine.com/intelligent-design/thank-you-okfanriffic/#comment-494454 "Einstein's equation predicts that, as the astronaut reaches the singularity (of the black-hole), the tidal forces grow infinitely strong, and their chaotic oscillations become infinitely rapid. The astronaut dies and the atoms which his body is made become infinitely and chaotically distorted and mixed-and then, at the moment when everything becomes infinite (the tidal strengths, the oscillation frequencies, the distortions, and the mixing), spacetime ceases to exist." Kip S. Thorne - "Black Holes and Time Warps: Einstein's Outrageous Legacy" pg. 476 Near-Death Experiences: Putting a Darwinist's Evidentiary Standards to the Test - Dr. Michael Egnor - October 15, 2012 Excerpt: Indeed, about 20 percent of NDE's are corroborated, which means that there are independent ways of checking about the veracity of the experience. The patients knew of things that they could not have known except by extraordinary perception -- such as describing details of surgery that they watched while their heart was stopped, etc. Additionally, many NDE's have a vividness and a sense of intense reality that one does not generally encounter in dreams or hallucinations.,,, The most "parsimonious" explanation -- the simplest scientific explanation -- is that the (Near Death) experience was real. Tens of millions of people have had such experiences. That is tens of millions of more times than we have observed the origin of species (or origin of life), which is never.,,, The materialist reaction, in short, is unscientific and close-minded. NDE's show fellows like Coyne at their sneering unscientific irrational worst. Somebody finds a crushed fragment of a fossil and it's earth-shaking evidence. Tens of million of people have life-changing spiritual experiences and it's all a big yawn. Note: Dr. Egnor is professor and vice-chairman of neurosurgery at the State University of New York at Stony Brook. http://www.evolutionnews.org/2012/10/near_death_expe_1065301.html "A recent analysis of several hundred cases showed that 48% of near-death experiencers reported seeing their physical bodies from a different visual perspective. Many of them also reported witnessing events going on in the vicinity of their body, such as the attempts of medical personnel to resuscitate them (Kelly et al., 2007)." Kelly, E. W., Greyson, B., & Kelly, E. F. (2007). Unusual experiences near death and related phenomena. In E. F. Kelly, E. W. Kelly, A. Crabtree, A. Gauld, M. Grosso, & B. Greyson, Irreducible mind (pp. 367-421). Lanham, MD: Rowman & Littlefield. Michaela's Amazing NEAR death experience - video http://www.youtube.com/watch?v=jTcHWz6UMZ8 Dr. Jeffrey Long: Just how strong is the evidence for a afterlife? - video http://www.youtube.com/watch?v=mptGAc3XWPs
Verse and Music:
Mark 8:37 Is anything worth more than your soul? Creed - My Own Prison http://www.youtube.com/watch?v=iBBqjGd3fHQ
bornagain77
I know, I love it. When I stop seeing your creationist nutjob friends on my campus screaming about how "Jesus loves me and....hates me" then I will stop being an ass to you guys. AVS
AVS, with all due respect, you are a jerk! bornagain77
Wiki warns you of that because they know its better to be safe than sorry. The fact of the matter is that wiki is plenty reliable for informal conversation. I use it frequently to supplement my learning in the classroom and as background for any topics I am unfamiliar with. I would venture it is correct 99% of the time. AVS
BA, you further prove my point that you simply do not have the necessary biological knowledge to carry out the conversations that you do. Protein function is a direct product of the protein's shape/form. You didn't "cause" any confusion, you only demonstrated your own. AVS
AVS How on earth do you find wiki good enough when wiki itself warns you about the unreliability of its content... Andre
Dr. Giem, my claim is that shape or form is only tenuously effected by sequential information, I said nothing about functionality. I'm well aware functionality is many times extremely sensitive point mutations. I'm sorry for any confusion I may have caused to this thread I have caused. And will comment no further.,,, I thought, and still think, the point I made towards form and shape to be important. Perhaps shadows of Aristotle drifting in the back of my mind. :) Matter and Form http://simplyphilosophy.org/philosophy/classical-greek-philosophy/aristotle/matter-and-form/ bornagain77
Also, wiki serves its purpose just fine for informal conversation. It is 99% accurate and for the most part up to date. And it most certainly does help me. Do I need to quote it again? AVS
Joe, for the last time, the chaperones are merely expediting the sequence based folding. Also, the different folds that can occur from an unchanged amino acid sequence are the product of sequence-based folding also, the variation comes from segments of the polypeptide strand exiting the ribosome at different rates. AVS
I see Paul, obviously at least some of the students have an understanding of the basics of evolution, the numbers don't lie. But I would suggest that you be careful about saying the "whole class" scored in the 99th percentile, as this is not what was said. What was said was that "students" scored in the 99th percentile. I would like to know if all their students took the test or was it just a select few? How many students were actually in the 99th percentile? Who else takes the test? I know my university doesn't require biology students to take tests like this. AVS
Wiki doesn't help you and it isn't a valid academic source. And without the chaperones the polypeptide would NOT find its required shape. So shut up already. With silent mutations the amino acid sequence is the same. And I already knew your explanation. That is why I said what I did. With the same amino acid sequence there can be different final proteins. Period, end of story. According to you that can't happen. Joe
AVS (#58), According to the website of Bryan College, it is part of the ETS Major Field Tests. Sounds like a standardized test to me, including mostly non-Christian schools. And it is not just one student, but the whole class. Now what do you think? Paul Giem
Joe, please read the first few paragraphs on the wiki page for chaperones, it will straighten you out as to how rare a process it is. You are still missing my point that the chaperones are merely catalyzing the sequence-based folding process. The folds are still dependent on amino acid sequence in the silent mutation's case. Let me explain, the association of certain tRNA to their codons slows the process of translation a bit more than other tRNA, this leads to the amino acid sequence outside of the ribosome maybe folding slightly differently because some of the amino acids that normally would have exited the ribosome with the normal nucleotide sequence, have not yet madde it out yet. In both this case, you will notice that folding is still being driven by the amino acid sequence. AVS
BA77, You are not optimally handling this situation. A. A protein with the sequence code for alanine aminotransferase will not perform the function of aspartate aminotransferase if we just fold it the right way. The sequence has to be changed also. The sequence may not be everything, but it is important. And don't forget, if you were to win this argument, you would destroy the argument that DNA must be at least approximately in the right sequence, and so fairly accurate DNA production is necessary for life. In other words, you would make it easier to argue for the spontaneous generation of life. It is not advisable for you to continue to press this point. DNA sequence is not everything, but it is not nothing, and it is not even minor. B. I had gotten AVS back to the original post. I want him (and others) to think about the idea that ID, and even Creationist, people can clearly understand evolution without accepting it. Now you are in the process of leading him down the same rabbit hole from which I had just extracted him, so he can argue your point rather than realize that sometimes "you just don't understand evolution" is not an adequate response. Look at the big picture. Paul Giem
AVS, it is NOT rare. And without the chaperones the polypeptide wouldn't fold. That is what has happened in most genetic engineering cases. Insulin was the rare success.
In the case of silent mutations altering translation speed and protein folding, this is still driven by the now changed DNA sequence.
It's the same amino acid sequence yet the folds are different. You sed the fold depends on the amino acid sequence. Obviously there is more to it than that. Your simpleton approach rivals that of middle-school students. Joe
A standardized test Paul? Which test is that? It sounds to me more like a general test the university gives its biology students as a requirement for graduation. And in a school full of creationists, it doesn't really surprise me that a creationist scored in the 99th percentile. AVS
Joe, we've already come to the agreement that it is rare and I've already stated that to my knowledge chaperones function by providing an environment in which the protein folds more easily, still driven by its amino acid sequence. Look up the Hsp60/Hsp10 complex. In the case of silent mutations altering translation speed and protein folding, this is still driven by the now changed DNA sequence. I'm not sure what your point is. AVS
Dr. Giem, If you are interested, I made a more thorough critique yesterday of why the sequential information in DNA has only ‘tenuous’ (weak or very slight) influence over shape and form in the DNA, cell, and over the overall body plan, here:
https://uncommondesc.wpengine.com/intelligent-design/jonathan-wells-far-from-being-all-powerful-dna-does-not-wholly-determine-biological-form/#comment-494620
Here are some more notes that extend the critique I made yesterday to include the materialistic processes of neo-Darwinism ever adequately explaining the shape or form of proteins:
Coherent Intrachain energy migration at room temperature - Elisabetta Collini and Gregory Scholes - University of Toronto - Science, 323, (2009), pp. 369-73 Excerpt: The authors conducted an experiment to observe quantum coherence dynamics in relation to energy transfer. The experiment, conducted at room temperature, examined chain conformations, such as those found in the proteins of living cells. Neighbouring molecules along the backbone of a protein chain were seen to have coherent energy transfer. Where this happens quantum decoherence (the underlying tendency to loss of coherence due to interaction with the environment) is able to be resisted, and the evolution of the system remains entangled as a single quantum state. http://www.scimednet.org/quantum-coherence-living-cells-and-protein/ Physicists Discover Quantum Law of Protein Folding – February 22, 2011 Quantum mechanics finally explains why protein folding depends on temperature in such a strange way. Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from. To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,, Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins. That's a significant breakthrough. Luo and Lo's equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics. http://www.technologyreview.com/view/423087/physicists-discover-quantum-law-of-protein/ INFORMATION AND ENERGETICS OF QUANTUM FLAGELLA MOTOR Hiroyuki Matsuura, Nobuo Noda, Kazuharu Koide Tetsuya Nemoto and Yasumi Ito Excerpt from bottom page 7: Note that the physical principle of flagella motor does not belong to classical mechanics, but to quantum mechanics. When we can consider applying quantum physics to flagella motor, we can find out the shift of energetic state and coherent state. http://www2.ktokai-u.ac.jp/~shi/el08-046.pdf
bornagain77
AVS, You said,
I can only imagine what this christian college gave their students to test their understanding of evolution.
It was a standardized test. You could deduce that from the use of 99th percentile. As Todd Wood (PhD) said here, " The 99th percentile means they're outperforming most students taught by actual evolutionists." Wouldn't you agree that at least some creationists understand evolution very well? Paul Giem
BTW there are alleged silent mutations in which the amino acid sequence remains the same but the protein misfolds. That couldn't happen if AVS was right. The misfolding has to do with the timing of the arrival of the tRNAs at the ribosome. Joe
AVS:
The bottom line is protein shape and function is entirely dependent on amino acid sequence.
Nope. Many proteins won't even take a 3D shape unless there are chaperones to make it so.
Even in the rare case of chaperones directly helping the folding process,
It isn't rare. Joe
Very true, if I have learned anything about biology it is that there is always an exception to the rule. But I think you would find it extremely difficult to find a process that doesn't rely on the amino acids of the protein to determine folding. To my knowledge chaperones function by making the proper folding process that is driven by the primary sequence more favorable. Also I think the native state of the pre-prion protein is more stable, the problem is when a specific part of the protein becomes unfolded, it cooperatively unfolds the rest of the protein and catalyzes more and more unfolding of more of that protein. that's my understanding. 99th percentile on the evolutionary biology...what? I can only imagine what this christian college gave their students to test their understanding of evolution. But anyways, yes i would need a lot more information than that post gave me to draw any conclusions. And I didn't watch the debate. I've wasted too much time being an asshole on here already to be watching other people do the same thing. AVS
AVS, You're mostly right. Always be careful of saying "always". ;) Protein shape is not "entirely" dependent on amino acid sequence. We don't know how rare chaperone help for folding is, but it definitely happens some of the time. A cause can be necessary without being sufficient. And the shape of the pre-prion protein is definitely not the most stable shape, or otherwise prions could not form. (And some of the bonds holding proteins in shape can be covalent, such as disulfide bonds.) Now that I have your attention, what do you think of the creationist class that scored 99th percentile on the evolutionary biology, and what did you think of the Nelson-Velasco debate? (Those were, after all, the subjects of the original post.) Paul Giem
Good point Paul, thanks. If amino acid sequence had as little of an effect on the final protein shape as BA would lead us to believe, we wouldn't see nearly as many enzyme malfunction diseases that can be traced directly back to a single amino acid mutation as we do. The bottom line is protein shape and function is entirely dependent on amino acid sequence. Even in the rare case of chaperones directly helping the folding process, the only reason the protein stays in that conformation after dissociating from the chaperone is because of the maintenance of noncovalent interactions between certain amino acids. AVS
Thanks for listening, BA77. You are essentially right about the need for chaperone proteins (of various kinds). My understanding is that without such proteins, cells die. They may not be needed for all protein folding, but they certainly are for a critical subset of protein folding. If you stick to that point, you'll get less, and less effective, diversionary tactics from opponents of ID. You are right, shape is, in many cases, not entirely dictated by sequence. Paul Giem
Thanks Dr. Geim for the salient criticism. And indeed I now agree that they were making far too strong of a claim with what they had. I wish now that I would have made that point more clear earlier, and thanks for calling me on it. But anyway, after looking and thinking the matter over for a bit, they could have made almost as strong of a statement and been correct. Remember AVS originally asked me this:
"I’m sorry BA, is that first article in your last post trying to say that the nucleotide sequence of a protein-coding gene has no effect on the final shape of the protein?"
And the answer to that specific question turns out to be that nucleotide sequence only has 'tenuous' influence on the final shape:
“It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true – the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous (very weak or slight) influence over their functions. ,,,,So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent. Stuart A. Newman, Ph.D. – Professor of Cell Biology and Anatomy http://www.desdeelexilio.com/2010/06/01/biologia-evolutiva-del-desarrollo-entrevista-a-stuart-a-newman/
Dr. Geim, I will remove that particular paper from my files since it is misleading as it is currently worded, but as to the point that AVS was originally trying to establish, that shape is dictated by sequence, what I've learned is that Darwinian processes, besides being unable to account for body plans (as Dr. Nelson pointed out Saturday), are also almost stopped dead in their tracks right out of the starting gate when it comes to trying to explain protein structure, much less explaining the higher levels of structural organization in an organism. bornagain77
bornagain77, A lot of ink and attention has been spilled unnecessarily, and perhaps by design. Remember that the original post remarked on the Nelson-Velasco debate. Proper questions might have included the one posed by mtcarner (#46). Is the debate available to the general public? The original post went on to mention the students at Bryan College, who are at a creationist (not just ID) college where they are taught by a creationist (not just ID) teacher, and were able to perform at the 99th percentile on a test on evolution. Presumably they "really understand evolution". Remarks on that would be on topic. Instead, after you posted in #4 and #5, a long series of articles with summaries, AVS called attention to one of your summaries, namely this one in #5:
A challenge to the genetic interpretation of biology – Feb 19, 2014 When a gene, a string of bases on the DNA molecule, is deployed, it is first transcribed and then translated into a peptide – a string of amino acids. To give rise to biological properties it needs to “fold” into a protein. This process consumes energy and is therefore governed by the 2nd law, but also by the environment in which the folding takes place. These two factors mean that there is no causal relationship between the original gene coding sequence and the biological activity of the protein. http://phys.org/news/2014-02-genetic-biology.html
He argued that the gene sequence does relate to the biological activity of the protein. You then defended your source, and he defended his argument, resulting in some 40 posts of back and forth that drew attention away from the salient points that were made by the original post. It is tempting to draw the conclusion that his intent was to derail the comments, which were heading in an uncomfortable (for him) direction, and you have (I assume unintentionally) assisted him. He chose a very soft target. Not only is it not true that "there is no causal relationship between the original gene coding sequence and the biological activity of the protein", but the original paper goes on to say that "Yes, a Nordic study of twins conducted in 2000 showed there was no evidence that cancer was a "genetic" disease – that is – that genes play no role in the causation of cancer. A wider international study involving 50,000 identical twin pairs published in 2012, showed that this conclusion applied to other common disease as well." These statements are simply in error. You don't have to take my word for it. Ever heard of BRCA1 and BRCA2? Familial polyposis coli? For that matter, ever heard of sickle cell anemia? To say that genes play no role in cancer or other common diseases is just balderdash. Now if the people writing had been more circumspect, and said that most cancers are not genetically determined, and most other common diseases are not genetically determined, they would have had a point. Even in the case of phenylketonuria, or PKU, clearly a genetic disease, diet makes a tremendous difference in the severity of the disease, with diets low in phenylalanine allowing people with the genetic defect to lead apparently otherwise normal lives. But the abstract and the article make too strong claims, and AVS was correct to challenge the article. Your first instinct was to defend the article because it was written by two PhD's in physics. As you said in #35,
Now I don’t know exactly how strong their case is for that specific claim, but considering that that are both physics professors,,,
The authors, Arto Annila, Professor of physics at Helsinki University and Keith Baverstock, Docent and former professor at the University of Eastern Finland,
and considering that you, AVS, are a committed Darwinist on a blog insulting people who disagree with you, then I’m also reasonably confident that these distinguished physics professors have done their homework and that they are not just whistling Dixie when they make such a dramatic claim that there is a severe disconnect between sequence and biological activity. And I am also confident that you are just trying to protect Darwinian claims by the usual non-substantive bluff, bluster and ad hominem that is typical of Darwinists.
But this is one case where your instincts were wrong. I won't pretend to know why the authors were wrong (insufficient evidence, hyperbole, narrow scientific training, being tired?), but they were. And it is best to admit it up front when you discover it, and even thank the objector for the information. If you had, AVS would have either had to graciously acknowledge the thanks, shut up, or taunt you, the latter putting him (her?) in the position of looking childish. And you could have pointed him back to the main point of the post, for which he has no good answer. There are three takeaway messages. First, take this particular paper out of your collection of quotable papers. Second, if someone challenges you, even if he or she is on the other side, take the challenge seriously and reply softly. And finally, double-check anything you find (even my videos!). Paul Giem
I was travelling Saturday afternoon and was unable to watch the debate. I was wondering if it is archived somewhere to watch? mtcarner
AVS- Look up "August Weismann"- he was key to modern evolutionists' thought. Joe
AVS:
No, Joe. Evolution does not “require that genes be everything.”
That is the ONLY parts that change and can change the organism- according to evos. But anyway do tell- what else changes and can cause the organism to change? Joe
The Fate of Darwinism: Evolution After the Modern Synthesis - David J. Depew and Bruce H. Weber - 2011 Excerpt: We trace the history of the Modern Evolutionary Synthesis, and of genetic Darwinism generally, with a view to showing why, even in its current versions, it can no longer serve as a general framework for evolutionary theory. The main reason is empirical. Genetical Darwinism cannot accommodate the role of development (and of genes in development) in many evolutionary processes.,,, http://www.springerlink.com/content/845x02v03g3t7002/ With a Startling Candor, Oxford Scientist Admits a Gaping Hole in Evolutionary Theory - November 2011 Excerpt: As of now, we have no good theory of how to read [genetic] networks, how to model them mathematically or how one network meshes with another; worse, we have no obvious experimental lines of investigation for studying these areas. There is a great deal for systems biology to do in order to produce a full explanation of how genotypes generate phenotypes,,, http://www.evolutionnews.org/2011/11/with_a_startling_candor_oxford052821.html The next evolutionary synthesis: Jonathan BL Bard (2011) Excerpt: We now know that there are at least 50 possible functions that DNA sequences can fulfill [8], that the networks for traits require many proteins and that they allow for considerable redundancy [9]. The reality is that the evolutionary synthesis says nothing about any of this; for all its claim of being grounded in DNA and mutation, it is actually a theory based on phenotypic traits. This is not to say that the evolutionary synthesis is wrong, but that it is inadequate – it is really only half a theory! http://www.biosignaling.com/content/pdf/1478-811X-9-30.pdf The Origin at 150: is a new evolutionary synthesis in sight? - Koonin - Nov. 2009 Excerpt: The edifice of the modern synthesis has crumbled, apparently, beyond repair. http://www.arn.org/blogs/index.php/literature/2009/11/18/not_to_mince_words_the_modern_synthesis Die, selfish gene, die - The selfish gene is one of the most successful science metaphors ever invented. Unfortunately, it’s wrong - Dec. 2013 Excerpt: But 15 years after Hamilton and Williams kited [introduced] this idea, it was embraced and polished into gleaming form by one of the best communicators science has ever produced: the biologist Richard Dawkins. In his magnificent book The Selfish Gene (1976), Dawkins gathered all the threads of the modern synthesis — Mendel, Fisher, Haldane, Wright, Watson, Crick, Hamilton, and Williams — into a single shimmering magic carpet (called the selfish gene). Unfortunately, say Wray, West-Eberhard and others, it’s wrong. https://uncommondesc.wpengine.com/darwinism/epigenetics-dawkins-selfish-gene-discredited-by-still-more-scientists-you-should-have-heard-of/ Modern Synthesis Of Neo-Darwinism Is False – Denis Nobel – video http://www.metacafe.com/w/10395212 ,, In the preceding video, Dr Nobel states that around 1900 there was the integration of Mendelian (discrete) inheritance with evolutionary theory, and about the same time Weismann established what was called the Weismann barrier, which is the idea that germ cells and their genetic materials are not in anyway influenced by the organism itself or by the environment. And then about 40 years later, circa 1940, a variety of people, Julian Huxley, R.A. Fisher, J.B.S. Haldane, and Sewell Wright, put things together to call it ‘The Modern Synthesis’. So what exactly is the ‘The Modern Synthesis’? It is sometimes called neo-Darwinism, and it was popularized in the book by Richard Dawkins, ‘The Selfish Gene’ in 1976. It’s main assumptions are, first of all, is that it is a gene centered view of natural selection. The process of evolution can therefore be characterized entirely by what is happening to the genome. It would be a process in which there would be accumulation of random mutations, followed by selection. (Now an important point to make here is that if that process is genuinely random, then there is nothing that physiology, or physiologists, can say about that process. That is a very important point.) The second aspect of neo-Darwinism was the impossibility of acquired characteristics (mis-called “Larmarckism”). And there is a very important distinction in Dawkins’ book ‘The Selfish Gene’ between the replicator, that is the genes, and the vehicle that carries the replicator, that is the organism or phenotype. And of course that idea was not only buttressed and supported by the Weissman barrier idea, but later on by the ‘Central Dogma’ of molecular biology. Then Dr. Nobel pauses to emphasize his point and states “All these rules have been broken!”. Professor Denis Noble is President of the International Union of Physiological Sciences. At the 10:30 minute mark of the following video, Dr. Trifonov states that the concept of the selfish gene 'inflicted an immense damage to biological sciences', for over 30 years: Second, third, fourth… genetic codes - One spectacular case of code crowding - Edward N. Trifonov - video https://vimeo.com/81930637 How life changes itself: the Read-Write (RW) genome. - 2013 Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences. http://www.ncbi.nlm.nih.gov/pubmed/23876611 etc.. etc.. bornagain77
No, Joe. Evolution does not "require that genes be everything." If you got your information from scientific sources and not the likes of the people on here at UD, you would know this. AVS
AS:
It is well known that genes are not everything, but they are very important.
Evolutionism requires that genes be everything as that is the only part they say makes all the required changes. If genes aren't everything then evolutionism fails. Joe
AVS"
Now as you’ll notice I quoted wiki four times, Joe, all of them supporting me.
And I provided a quote from YOUR wiki reference that supports me. Heck you don't even undersstand what I am saying and your wiki page doesn't even address it. You lose because you are ignorant due to your anger.
You took the first sentence of the page because it helped your argument.
True and you don't even know what my argumant is.
Obviously the first sentence is going to list everything that chaperones do.
As I said you have no idea what my argument is. I never said all chaperones do is fold proteins. You have serious issues and should seek help.
For the last time, the majority of chaperones do not help proteins fold.
What a jerk you are. I never said anything to the contrary. All I said was there are proteins that canNOT fold by themselves. As I said its as if you are proud to be an ass. Nice job Joe
Of related note:
"It was long believed that a protein molecule’s three-dimensional shape, on which its function depends, is uniquely determined by its amino acid sequence. But we now know that this is not always true – the rate at which a protein is synthesized, which depends on factors internal and external to the cell, affects the order in which its different portions fold. So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous (very weak or slight) influence over their functions. ,,,,So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used. Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent. Stuart A. Newman, Ph.D. - Professor of Cell Biology and Anatomy http://www.desdeelexilio.com/2010/06/01/biologia-evolutiva-del-desarrollo-entrevista-a-stuart-a-newman/
bornagain77
I have plenty of respect for physics and physicists, queerius, but I also understand how much effort goes into becoming a PhD in a specific field and how that means you are specialized in that specific field. While I don't doubt they know a god deal of biology, I am confident in my own knowledge of biology. Like I said to BA, some of the things they said in the article did not seem to make sense. And most of what BA says does not make sense either so I have a feeling you're trying to pick a fight. If so, please go ahead and explain how anything I have said is wrong. AVS
Bornagain77, You have way more patience than I do! If AVS were a physical chemist, I think he would have more respect for physics. The issue that AVS is misunderstanding concerns causality (versus correlation) and heritability. Your posts as usual are nicely organized and present interesting developments that anyone who claims they're working on cancer research should be familiar with. Obviously, AVS skimmed your posts and is not familiar with these discoveries. I appreciate your effort. Thank you! -Q Querius
First of all BA, you don't know anything about me. Also, I think I'd be pretty comfortable comparing my knowledge of biology to that of these two physics professors. I highly doubt these two have the evidence to back the claim that "there is no causal relationship between the original gene coding sequence and the biological activity of the protein." Unless I'm reading it wrong which I don't think I am. Also, the fact that they say "genes play no role in cancer" makes my highly suspicious, as that would disagree with many a lot of research done throughout the last half-century. Not to mention the fact that they say "it has not proved possible to relate abnormal gene sequences to common diseases" which unless again I am misreading, is completely and utterly false. We have traced hundreds of diseases back to single mutations in protein coding sequences. It is well known that genes are not everything, but they are very important. AVS
AVS, unlike you, I do not pretend to know all the answers beforehand. Although I do know for a fact that Darwinian processes are grossly inadequate to explain the unfathomed levels of complexity we are finding in molecular biology. Indeed molecular biology is a very, very, complicated field of study and anyone who thinks he has most everything figured out in molecular biology is severely deluding himself.
Systems biology: Untangling the protein web - July 2009 Excerpt: Vidal thinks that technological improvements — especially in nanotechnology, to generate more data, and microscopy, to explore interaction inside cells, along with increased computer power — are required to push systems biology forward. "Combine all this and you can start to think that maybe some of the information flow can be captured," he says. But when it comes to figuring out the best way to explore information flow in cells, Tyers jokes that it is like comparing different degrees of infinity. "The interesting point coming out of all these studies is how complex these systems are — the different feedback loops and how they cross-regulate each other and adapt to perturbations are only just becoming apparent," he says. "The simple pathway models are a gross oversimplification of what is actually happening." http://www.nature.com/nature/journal/v460/n7253/full/460415a.html
But I manage to muddle my way through it in spite of Darwinian attempts to obfuscate matters as you have done in this post. Moreover AVS, contrary to your claim that protein folding is well understood and that 'proteins will fold on their own', the fact of the matter, as is evident from protein isoforms, is that proteins are multifunctional, taking on different functions, and I strongly suspect different nuances of shape, depending on what cellular environment and/or context they are in. I had already listed several studies pointing out that structural information in the cell is just as, in not more, important as the linear sequences on DNA. But the point of the particular paper that you are contesting states the disconnect between structure and sequence in much stronger language,,,
A challenge to the genetic interpretation of biology – Feb 19, 2014 When a gene, a string of bases on the DNA molecule, is deployed, it is first transcribed and then translated into a peptide – a string of amino acids. To give rise to biological properties it needs to “fold” into a protein. This process consumes energy and is therefore governed by the 2nd law, but also by the environment in which the folding takes place. These two factors mean that there is no causal relationship between the original gene coding sequence and the biological activity of the protein. http://phys.org/news/2014-02-genetic-biology.html
Now I don't know exactly how strong their case is for that specific claim, but considering that that are both physics professors,,,
The authors, Arto Annila, Professor of physics at Helsinki University and Keith Baverstock, Docent and former professor at the University of Eastern Finland,
and considering that you, AVS, are a committed Darwinist on a blog insulting people who disagree with you, then I'm also reasonably confident that these distinguished physics professors have done their homework and that they are not just whistling Dixie when they make such a dramatic claim that there is a severe disconnect between sequence and biological activity. And I am also confident that you are just trying to protect Darwinian claims by the usual non-substantive bluff, bluster and ad hominem that is typical of Darwinists. But now that I've re-read the article 'A challenge to the genetic interpretation of biology', it is interesting to point out the empirical evidence they cited:
Is there any empirical evidence to support this? Yes, a Nordic study of twins conducted in 2000 showed there was no evidence that cancer was a "genetic" disease – that is – that genes play no role in the causation of cancer. A wider international study involving 50,000 identical twin pairs published in 2012, showed that this conclusion applied to other common disease as well. Since the sequencing of the human genome was completed in 2001 it has not proved possible to relate abnormal gene sequences to common diseases giving rise to the problem of the "missing heritability".
The reason I find their empirical support interesting is that it is now known that, in direct contradiction to the reductionist model of Darwiniam, even 'mental states' can epigentically alter gene expression.
Scientists Finally Show How Your Thoughts Can Cause Specific Molecular Changes To Your Genes, - December 10, 2013 Excerpt: “To the best of our knowledge, this is the first paper that shows rapid alterations in gene expression within subjects associated with mindfulness meditation practice,”,,, “Most interestingly, the changes were observed in genes that are the current targets of anti-inflammatory and analgesic drugs,”,,, the researchers say, there was no difference in the tested genes between the two groups of people at the start of the study. The observed effects were seen only in the meditators following mindfulness practice. In addition, several other DNA-modifying genes showed no differences between groups, suggesting that the mindfulness practice specifically affected certain regulatory pathways. http://www.tunedbody.com/scientists-finally-show-thoughts-can-cause-specific-molecular-changes-genes/
Now AVS, perhaps you may say, 'Wow, we are not complete victims of our genes after all' as I did when I saw that study, which would be a pleasant surprise, but something tells me that a reasonable response like that will not come from you. Proverbs 17:22 A cheerful heart is good medicine, but a crushed spirit dries up the bones. bornagain77
Yes, Moose doc, next time I want to know about what really matters in biology, I will come to you. You seem to be just as knowledgeable about this topic as BA is. AVS
Gents (I assume gender) this yapity yap is pretty lame. Who cares if chaperones do stuff other than help proteins fold. Who cares if many proteins fold without the aid of chaperones. From what I can tell, the whole case of proteins and chaperones is fully valid if one of the tasks of chaperones is to fold proteins, and if some proteins require the assistance of chaperones for folding. Moose Dr
Oh BA, you are so worldly with your quotes on high. It almost makes me think you know what you are talking about. Almost. There might be a lot of things we don't know, but we certainly do know a fair amount. I think it's about time we admit that we know that we have evolved from a common ancestor, the how exactly, is what we don't know. AVS
‘We are so woefully ignorant about how biology really works. We still don’t understand how a particular DNA sequence—when we just stare at it—codes for a protein that has a particular function. We can’t even figure out how that protein would fold—into what kind of three-dimensional shape. And I would defy anybody who is going to tell me that they could, from first principles, predict not only the shape of the protein but also what it does.’ - Francis Collins – Former Director of the Human Genome Project bornagain77
Unpleasant only because you can't deal with someone who calls you on your BS. I'm sure you don't get that a lot when you cater to the scientifically illiterate. Have a nice night. <3 AVS
Well AVS, that's enough insult for me tonight. You are a very unpleasant person to deal with. But anyways, May the God who created you, fearfully and wonderfully, bless you richly! bornagain77
No, the answer I got was that you had no idea what you were talking about and probably haven't even read the paper. Is that what you're doing now while you copy and paste more nonsense? Seriously, waht do those two articles have to do with the conversation. It would help if you added some of your own dialogue to your copy and paste posts. And it would definitely make me feel like you actually read the articles you are quoting. AVS
I'm not sure what your problem with wiki is. It is obviously not a reliable source if I am writing a scientific paper, but for you guys it does its job very well and I would venture a guess that wiki is over 90% accurate for everything it says. Now as you'll notice I quoted wiki four times, Joe, all of them supporting me. You took the first sentence of the page because it helped your argument. Obviously the first sentence is going to list everything that chaperones do. Now if you'll look at my four quotes, you'll see that helping proteins fold is not the only thing that chaperones do, in fact it is only a small portion of what chaperones do. You'll also notice that it says something about most proteins being able to fold on their own. Ring any bells? Also notice how the paper you cited is specifically talking about chaperones that aid protein folding. Of course they are going to mention the fact that chaperones help proteins fold. For the last time, the majority of chaperones do not help proteins fold. They serve many other functions and only a fraction off all proteins require chaperones to fold correctly. AVS
AVS, "To which I got the answer I was looking for anyway" Let me guess, Let me guess,,, The answer you knew beforehand was 'Evolution did it'! Human Genes: Alternative Splicing (For Proteins) Far More Common Than Thought: Excerpt: two different forms of the same protein, known as isoforms, can have different, even completely opposite functions. For example, one protein may activate cell death pathways while its close relative promotes cell survival. http://www.sciencedaily.com/releases/2008/11/081102134623.htm Genes Code For Many Layers of Information - They May Have Just Discovered Another - Cornelius Hunter - January 21, 2013 Excerpt: “protein multifunctionality is more the rule than the exception.” In fact, “Perhaps all proteins perform many different functions by employing as many different mechanisms." http://darwins-god.blogspot.com/2013/01/genes-code-for-many-layers-of.html bornagain77
Ah yes, the ol' "demonstrate the origination of a molecular machine" demands. I knew you'd go back to your old ways. You are quite the character. I don't think anybody is a fool for doubting anything. I think they're a fool when they ignore facts and live in a fantasy world. I asked you a simple question at the start and you have failed to answer it multiple times. You aren't going to go through the details because you either didn't read the paper or you don't understand it. And yet you chose to try to use it as evidence for your argument. I was simply being skeptical, and asked a question. To which I got the answer I was looking for anyways. AVS
Wikipedia:
In molecular biology, molecular chaperones are proteins that assist the non-covalent folding or unfolding and the assembly or disassembly of other macromolecular structures.
Joe
Only small proteins can fold on their own and the median length is well over that limit. Joe
OH goody we got the smug Darwinian expert quoting wiki to us now! Perhaps he can find some help from talkorigins while he is at it! :) bornagain77
Really AVS- are you talking about blind watchmaker evolution? If so please do elaborate. Joe
Wikipedia? Really? Protein Folding and Chaperones
Abstract Proteins fold via specific pathways to achieve their native structure. Protein structures are, however, inherently unstable; hence folding and unfolding are in equilibrium. Protein instability is a major concern inside the cell. Specialised proteins called molecular chaperones are, therefore, required to assist proteins in folding and to prevent aggregation of folding intermediates. Many different classes of chaperones exist that are conserved throughout all kingdoms of life, many of which are known as heat?shock proteins. Chaperones typically recognise hydrophobic patches, but the exact functions and mechanisms of action of the various chaperone classes are very different. The main chaperone classes Hsp70, Hsp90, Hsp100 and chaperonins all depend on adenosine triphosphatase (ATPase) cycles, which enable subtle activity control by co?chaperones. The molecular understanding of the mechanism of both chaperones and protein folding are key problems in today's life sciences. The importance is illustrated by the fact that many diseases are associated with these processes.
Joe
Really Joe? You should just see yourself out now. Quit while your ahead bud. But not really AVS
Why yes AVS, Darwinism can do all things. Even things that are completely antithetical to basic precepts of Darwinism, and you think everybody else is a fool for doubting Darwinism even though you cannot demonstrate the origination of a single molecular machine by Darwinian processes. Go figure. I call it making excuses! PS, why in blue blazes do you keep asking me my opinion on the paper when you already think you know all the answers? I'm certainly not going to go through the details with you, especially considering the typical condescending way you treat people who disagree with you. bornagain77
Joe, you are on the internet. Go to the wiki page for chaperones..you know what I'll do it for you. Here are some excerpts: "The common perception that chaperones are concerned primarily with protein folding is incorrect." "One major function of chaperones is to prevent both newly synthesised polypeptide chains and assembled subunits from aggregating into nonfunctional structures." Only a small subset of chaperones are highly specific 'steric chaperones' and convey unique structural (steric) information onto proteins, which cannot be folded spontaneously " Other chaperones are involved in folding newly made proteins as they are extruded from the ribosome. Although most newly synthesized proteins can fold in absence of chaperones, a minority strictly requires them for the same." Did you get that? MOST proteins can fold on their own. A MINORITY require chaperones. Don't go by what your high school biology book said, it made the mistake of over simplifying things for the laypeople. AVS
What does "over the course of evolution" mean? Joe
So you're abandoning our first topic and bringing up a bacteria that can both live in an extreme environment and is able to repair its genome? Hmmm...do we really find that odd? You might want to plug your ears for this, but I would assume that over the course of evolution, an organism that is now able to live in an extreme environment would be pretty good at repairing its DNA, keeping proteins folded, and maintaining cellular integrity. No? Call me crazy. AVS
Chaperones are used to get proteins to fold- long proteins. IOW you are wrong again. Joe
So AVS, sequential information is primary in your book? Explain how the following is possible from the reductive materialistic framework of neo-Darwinism: Extreme Genome Repair - 20 March 2009 Excerpt: If its naming had followed, rather than preceded, molecular analyses of its DNA, the extremophile bacterium Deinococcus radiodurans might have been called Lazarus. After shattering of its 3.2 Mb genome into 20–30 kb pieces by desiccation or a high dose of ionizing radiation, D. radiodurans miraculously reassembles its genome such that only 3 hr later fully reconstituted nonrearranged chromosomes are present, and the cells carry on, alive as normal. http://www.sciencedirect.com/science/article/pii/S0092867409002657 bornagain77
Very rarely are chaperones needed for correct protein folding. Chaperones are much more often used to hold proteins in their unfolded form so that they can be translocated into organelles such as the mitochondria. They are also often used in times of stress to stop unfolded proteins from aggregating. Prions are a rare case of protein aggregation, and in my opinion are a good example of what I would call "poor design." Anything else you guys care to be wrong about? AVS
I'm downplaying the problem? What problem is that? Fig. 4? Where's that? Oh you copy and pasted again, gotcha. All I'm saying is that a lot of proteins are completely capable of folding on their own, driven by interactions of the primary sequence, without the help of chaperones. The folding of cytosolic and secreted proteins is governed by the burying of hydrophobic residues within the core of the protein and by the electrostatic interactions between charged residues. Each amino acid also tends to have certain bond rotation angles which are more entropically favorable, often driving the protein folding in certain directions. Proteins with multiple domains typically fold in a stepwise fashion, not all at one. The vast majority of protein folding is governed by the amino acid sequence, which is the direct product of translation of the nucleotide sequence. Now for the last time, is the source you originally cited trying to say that this is not true? Or is it that you have no idea what you are talking about. Or both? AVS
Yes the nucleotide sequence of a protein coding gene has an effect on the shape. However many proteins require chaperones in order for them to find their shape. And without chaperones they would just be like wet spaghetti, just a lot smaller. That means you need the right amino acid sequence AND the right chaperone(s) to get the required protein. And even then prions demonstrate that existing proteins can take on new/ different shape Joe
AVS, you are downplaying the problem. Why? This understanding of protein folding was obtained from computer models (in silico) or from experiments in the laboratory (in vitro) in which an individual protein was denatured to observe it folding back into its original form. But, the situation is considerably more complex in the living cell (in vivo). Although the fundamental energy rules also apply here, folding at least of large proteins rarely takes place spontaneously, as the ribosomes do not synthesize only one protein at a time. Instead, cells contain a vast number of proteins and other biomolecules at the extraordinarily high concentration of 340 grams per litre. Ordered protein folding in this cramped chaos is only possible under the supervision of specialized molecules, called chaperones, which accompany proteins and make sure that those that are being formed at the ribosomes do not clump together prematurely (Fig. 4). Chaperones do not merely oversee the folding of the protein, they also protect its tertiary structure in situations in which the cell is under stress; for example, elevated body temperature, so these chaperones have also been classified as heat-shock proteins (HSPs). bornagain77
Whoa whoa whoa pump the brakes there BA. Was that a reply to my question? I can't tell, probably because 99% of it isn't even your own words. I'm going to ask one more time. Does that article you cited claim that the nucleotide sequence of a protein coding gene has no effect on the final shape of the protein? Did you even read the article? You do know that we can purify proteins, completely unfold them, and then refold them to their natural conformation right? Protein folding is largely driven by the amino acid sequence, which is entirely dependent on the nucleotide sequence within DNA. Do you have any idea what I am talking about and what you are trying to talk about? AVS
of note: Although it is possible to deduce the primary structure of a protein from a gene's sequence, its tertiary structure cannot be determined (although it should become possible to make predictions when more tertiary sequences are submitted to databases). It can only be determined by complex experimental analyses and, at present, this information is only known for about 10% of proteins. http://www.nature.com/horizon/proteinfolding/background/importance.html The primary structure of a peptide or protein is the linear sequence of its amino acid structural units, and partly comprises its overall biomolecular structure. http://en.wikipedia.org/wiki/Protein_primary_structure The term protein tertiary structure refers to a protein's geometric shape. http://en.wikipedia.org/wiki/Protein_tertiary_structure Francis Collins on Making Life Excerpt: 'We are so woefully ignorant about how biology really works. We still don't understand how a particular DNA sequence—when we just stare at it—codes for a protein that has a particular function. We can't even figure out how that protein would fold—into what kind of three-dimensional shape. And I would defy anybody who is going to tell me that they could, from first principles, predict not only the shape of the protein but also what it does.' - Francis Collins - Former Director of the Human Genome Project http://www.pbs.org/wgbh/nova/tech/collins-genome.html Protein folding makes Rubik's cube seem like child's play by comparison: The Humpty-Dumpty Effect: A Revolutionary Paper with Far-Reaching Implications - Paul Nelson - October 23, 2012 Excerpt: Put simply, the Levinthal paradox states that when one calculates the number of possible topological (rotational) configurations for the amino acids in even a small (say, 100 residue) unfolded protein, random search could never find the final folded conformation of that same protein during the lifetime of the physical universe. http://www.evolutionnews.org/2012/10/a_revolutionary065521.html Thus I re-reference the quantum protein folding paper: Physicists Discover Quantum Law of Protein Folding – February 22, 2011 Quantum mechanics finally explains why protein folding depends on temperature in such a strange way. Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from. To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,, Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins. That’s a significant breakthrough. Luo and Lo’s equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics. http://www.technologyreview.com/view/423087/physicists-discover-quantum-law-of-protein/ bornagain77
I'm sorry BA, is that first article in your last post trying to say that the nucleotide sequence of a protein-coding gene has no effect on the final shape of the protein? AVS
This following recent paper really brought this point home:
A challenge to the genetic interpretation of biology - Feb 19, 2014 When a gene, a string of bases on the DNA molecule, is deployed, it is first transcribed and then translated into a peptide – a string of amino acids. To give rise to biological properties it needs to "fold" into a protein. This process consumes energy and is therefore governed by the 2nd law, but also by the environment in which the folding takes place. These two factors mean that there is no causal relationship between the original gene coding sequence and the biological activity of the protein. http://phys.org/news/2014-02-genetic-biology.html
Moreover, this following paper shows that protein folding is, in large measure, governed by 'spooky' quantum processes, and is not governed solely by 'classical' processes.
Physicists Discover Quantum Law of Protein Folding – February 22, 2011 Quantum mechanics finally explains why protein folding depends on temperature in such a strange way. Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from. To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,, Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins. That's a significant breakthrough. Luo and Lo's equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics. http://www.technologyreview.com/view/423087/physicists-discover-quantum-law-of-protein/
The failure of 'form' to be reduced to neo-Darwinian processes is not just some minor nitpicking on neo-Darwinian processes but is a failure for neo-Darwinism at the most basic level of explanation for what it seeks to explain. Namely that there is a correspondence to the linear sequences on DNA and form. I think Talbott has dome a excellent job of elucidating just how problematic trying to explain 'form' is for Darwinists:
HOW BIOLOGISTS LOST SIGHT OF THE MEANING OF LIFE — AND ARE NOW STARING IT IN THE FACE - Stephen L. Talbott - May 2012 Excerpt: “If you think air traffic controllers have a tough job guiding planes into major airports or across a crowded continental airspace, consider the challenge facing a human cell trying to position its proteins”. A given cell, he notes, may make more than 10,000 different proteins, and typically contains more than a billion protein molecules at any one time. “Somehow a cell must get all its proteins to their correct destinations — and equally important, keep these molecules out of the wrong places”. And further: “It’s almost as if every mRNA [an intermediate between a gene and a corresponding protein] coming out of the nucleus knows where it’s going” (Travis 2011),,, Further, the billion protein molecules in a cell are virtually all capable of interacting with each other to one degree or another; they are subject to getting misfolded or “all balled up with one another”; they are critically modified through the attachment or detachment of molecular subunits, often in rapid order and with immediate implications for changing function; they can wind up inside large-capacity “transport vehicles” headed in any number of directions; they can be sidetracked by diverse processes of degradation and recycling... and so on without end. Yet the coherence of the whole is maintained. The question is indeed, then, “How does the organism meaningfully dispose of all its molecules, getting them to the right places and into the right interactions?” The same sort of question can be asked of cells, for example in the growing embryo, where literal streams of cells are flowing to their appointed places, differentiating themselves into different types as they go, and adjusting themselves to all sorts of unpredictable perturbations — even to the degree of responding appropriately when a lab technician excises a clump of them from one location in a young embryo and puts them in another, where they may proceed to adapt themselves in an entirely different and proper way to the new environment. It is hard to quibble with the immediate impression that form (which is more idea-like than thing-like) is primary, and the material particulars subsidiary. Two systems biologists, one from the Max Delbrück Center for Molecular Medicine in Germany and one from Harvard Medical School, frame one part of the problem this way: "The human body is formed by trillions of individual cells. These cells work together with remarkable precision, first forming an adult organism out of a single fertilized egg, and then keeping the organism alive and functional for decades. To achieve this precision, one would assume that each individual cell reacts in a reliable, reproducible way to a given input, faithfully executing the required task. However, a growing number of studies investigating cellular processes on the level of single cells revealed large heterogeneity even among genetically identical cells of the same cell type. (Loewer and Lahav 2011)",,, And then we hear that all this meaningful activity is, somehow, meaningless or a product of meaninglessness. This, I believe, is the real issue troubling the majority of the American populace when they are asked about their belief in evolution. They see one thing and then are told, more or less directly, that they are really seeing its denial. Yet no one has ever explained to them how you get meaning from meaninglessness — a difficult enough task once you realize that we cannot articulate any knowledge of the world at all except in the language of meaning.,,, http://www.netfuture.org/2012/May1012_184.html#2
All of which begs the question, if Darwinists cannot give a coherent explanation for how even one organism is achieving its final 'form' during it's embryological development, then what in blue blazes gives Darwinists the audacity to tell us that they know for a fact how all life originated on earth?
Scant search for the Maker Excerpt: But where is the experimental evidence? None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of 20 to 30 minutes, and populations achieved after 18 hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another, in spite of the fact that populations have been exposed to potent chemical and physical mutagens and that, uniquely, bacteria possess extrachromosomal, transmissible plasmids. Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic to eukaryotic cells, let alone throughout the whole array of higher multicellular organisms. - Alan H. Linton - emeritus professor of bacteriology, University of Bristol. http://www.timeshighereducation.co.uk/story.asp?storycode=159282
Verse and Music:
Psalm 139:13 For you created my inmost being; you knit me together in my mother's womb. Mandisa - Esther - Born For This - music video http://www.youtube.com/watch?v=ZxFCber4TDo
bornagain77
I thought Dr. Nelson, considering the limited time in such a format, did a fine job in today's debate. Dr. Velasco, for his part, seemed to think simply 'believing' in common descent is more important than an actual empirical demonstration that his proposed Darwinian mechanism of Natural Selection and Random Variation/Mutation is up to the task he has attributed to it. Dr. Nelson clearly showed to the audience that his proposed Darwinian mechanism of Natural Selection and Random Variation/Mutation is NOT up to the task he has attributed to it. Dr. Nelson's main point was a condensed version of this talk:
Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth (excellent update) – video Text from one of the Saddleback slides: 1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows. 2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring. 3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo. Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes. http://www.saddleback.com/mc/m/7ece8/ Response to John Wise - October 2010 Excerpt: A technique called "saturation mutagenesis"1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans--because none of the observed developmental mutations benefit the organism. http://www.evolutionnews.org/2010/10/response_to_john_wise038811.html
and this talk:
The Miracle of Development Part 1 - Origins with Dr. Paul A. Nelson - video - April 2013 http://www.youtube.com/watch?v=JD9qMvz6T90 The Miracle of Development Part 2 - Origins with Dr. Paul A. Nelson - video - April 2013 http://www.youtube.com/watch?v=Vz12PI3BkQ4
Darwinists simply do not have any empirical evidence that Darwinian processes can produce changes in body plans. Moreover, there is now a fairly strong case to be made that body plans are not reducible to the linear sequences on DNA, as is presupposed in neo-Darwinism, but that 'structural information' is its own separate source of information:
“Live memory” of the cell, the other hereditary memory of living systems - 2005 Excerpt: To understand this notion of “live memory”, its role and interactions with DNA must be resituated; indeed, operational information belongs as much to the cell body and to its cytoplasmic regulatory protein components and other endogenous or exogenous ligands as it does to the DNA database. We will see in Section 2, using examples from recent experiments in biology, the principal roles of “live memory” in relation to the four aspects of cellular identity, memory of form, hereditary transmission and also working memory. http://www.ncbi.nlm.nih.gov/pubmed/15888340 Not in the Genes: Embryonic Electric Fields - Jonathan Wells - December 2011 Excerpt: although the molecular components of individual sodium-potassium channels may be encoded in DNA sequences, the three-dimensional arrangement of those channels -- which determines the form of the endogenous electric field -- constitutes an independent source of information in the developing embryo. http://www.evolutionnews.org/2011/12/not_in_the_gene054071.html
This following peer-reviewed paper holds that there is a 'irreducible organizational complexity' between genetic (digital) information and epigenetic (analog/structural) information:
Refereed scientific article on DNA argues for irreducible complexity - October 2, 2013 Excerpt: This paper published online this summer is a true mind-blower showing the irreducible organizational complexity (author’s description) of DNA analog and digital information, that genes are not arbitrarily positioned on the chromosome etc.,, ,,,First, the digital information of individual genes (semantics) is dependent on the the intergenic regions (as we know) which is like analog information (syntax). Both types of information are co-dependent and self-referential but you can’t get syntax from semantics. As the authors state, “thus the holistic approach assumes self-referentiality (completeness of the contained information and full consistency of the different codes) as an irreducible organizational complexity of the genetic regulation system of any cell”. In short, the linear DNA sequence contains both types of information. Second, the paper links local DNA structure, to domains, to the overall chromosome configuration as a dynamic system keying off the metabolic signals of the cell. This implies that the position and organization of genes on the chromosome is not arbitrary,,, http://www.christianscientific.org/refereed-scientific-article-on-dna-argues-for-irreducibly-complexity/
The following papers hold that the genotype-phenotype mapping cannot be reduced to a genetic program encoded in DNA sequences:
Not Junk After All—Conclusion - August 29, 2013 Excerpt: Many scientists have pointed out that the relationship between the genome and the organism — the genotype-phenotype mapping — cannot be reduced to a genetic program encoded in DNA sequences. Atlan and Koppel wrote in 1990 that advances in artificial intelligence showed that cellular operations are not controlled by a linear sequence of instructions in DNA but by a “distributed multilayer network” [150]. According to Denton and his co-workers, protein folding appears to involve formal causes that transcend material mechanisms [151], and according to Sternberg this is even more evident at higher levels of the genotype-phenotype mapping [152]. https://uncommondesc.wpengine.com/junk-dna/open-mike-cornell-obi-conference-chapter-11-not-junk-after-all-conclusion/ The Types: A Persistent Structuralist Challenge to Darwinian Pan-Selectionism - Michael J. Denton - 2013 Excerpt: Cell form ,,,Karsenti comments that despite the attraction of the (genetic) blueprint model there are no “simple linear chains of causal events that link genes to phenotypes” [77: p. 255]. And wherever there is no simple linear causal chain linking genes with phenotypes,,,—at any level in the organic hierarchy, from cells to body plans—the resulting form is bound to be to a degree epigenetic and emergent, and cannot be inferred from even the most exhaustive analysis of the genes.,,, To this author’s knowledge, to date the form of no individual cell has been shown to be specified in detail in a genomic blueprint. As mentioned above, between genes and mature cell form there is a complex hierarchy of self-organization and emergent phenomena, rendering cell form profoundly epigenetic. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2013.3/BIO-C.2013.3
bornagain77
From now on, anyone who doesn't understand evolutionary theory needs only to ask the biology graduates of Brian College, or perhaps Todd Wood. I'm sure they will straighten him/her out. :D Paul Giem
Well loss of intellectual integrity, or indeed, a quasi-amoral ignorance of the very concept of intellectual integrity will necessarily wreak damage on the atheists' capacity for conceptual thought, and indeed, will continue to do so exponentially. Dumber and dumber. Hence, the named, mad professors who figure so much on UD as, well.. mad professors. The phenomenon is very apparent in the UK, with the result that a place in private religious schools is coveted by upwardly-mobile parents for their sprogs, and will even move home, to be close to the school in question, meet an important qualification criterion. Truth is stranger than fiction, but, faced with this shame, militant atheists are always clamouring for the religious schools to be closed down... on the grounds that they instil religious bigotry!!!! Axel
Warms my heart. I once represented a young college student who had been humiliated by her Darwinist prof. She announced that she should not have to learn Darwinian theory at all. I said to her that while I would defend her legal rights, I disagreed with that statement. I told her that as an anti-Darwinist she had an obligation to understand Darwinism better than the Darwinist she would inevitably encounter. How can she critique a theory she did not understand? Smug Darwinists (I sometimes wonder if there is any other kind) often tell me the only reason I disagree with them is that I don't understand the theory. I take delight (is that delight perverse? I'll let others decide) smacking that particular trope down every time it raises its ugly little whack-a-mole head. Barry Arrington

Leave a Reply