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Larry almost got it right, but he just can’t turn the corner

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In 2013 Larry wrote On Beating Dead Horses

I was reminded of this while reading Salvador Corova’s latest post on Uncommon Descent because he refers to beating dead horses [If not Rupe and Sanford’s presentation (8/6/13), would you believe Wiki? In this case, yes]. I’m not going to make any comments. Read it and weep for the IDiots.

Well, it turned out Larry did make comments in that very same thread. 🙂

Sal begins with …

Evolutionists reluctantly admit most evolution is free of selection and therefore non-Darwinian …

I’ve been trying to teach this to the IDiots for over twenty years. Yet they still insist on referring to evolution as “Darwinism” and they continue to ignore random genetic drift in their attacks on evolution. About 99% of all IDiots have no idea what Sal is talking about. (Sal Cordova doesn’t know either.)

What Sal is saying is that practically all of the mutations being fixed in humans are either neutral or slightly deleterious. That has implications. It strongly suggests that most of our genome is junk.

Not quite, but almost, let me re-write the previous paragraph with errors corrected:

What Sal is saying is that IF practically all of the mutations being fixed in humans are either neutral or slightly deleterious, that has implications. It strongly suggests that most of our genome WOULD BE junk.

Larry Moran (with errors edited out by Sal)

My argument follows the form of a Proof by Contradiction. As we find more evidence that the genome is not junk, then it falsifies the premise that all of the mutations were fixed by neutral evolution in the first place.

VJ and I agree on the final conclusion, but I pleaded that an alternate line of proof was needed to falsify Kimura/Nei’s version of neutral theory (neutral evolution all the way) in favor of ReMine/Sanford’s version of neutral theory (special creation + neutral evolution ).

If Larry believes that neutral evolution makes junk, this may lead to a logical contradiction depending on how neutral evolution makes junk. If making junk includes eroding existing function at a rate higher than creating function, then this falsifies neutral evolution and casts doubt on evolution in general as the mechanism that assembles design out of many damaging mutations.

Empirically speaking, with respect to function, most observed evolution in the lab and field is loss of function, therefore it seems that indeed the rate of function loss is outpacing rate of function acquisition. This is known as “Behe’s Rule.” I even quote one of Larry’s heroes, Koonin in the discussion of Behe’s Rule in reductive evolution of complexity.

These considerations lead to scientifically testable predictions related to ENCODE, junk DNA and deeply conserved sequences. If the deeply conserved sequences are evolving in the present day according to neutral evolution, then how did they arise in the first place and remain conserved? It might be difficult to test this because of the expense, but what might we find when it is eventually done right? I’ve predicted rise in Single Nucleotide Polymorphisms in conserved regions since January 2007 here. I discussed this idea with Dr. Sanford and Dr. Carter at ICC 2013, and they were enthusiastic about the testability of the idea.

The publication of my prediction in 2007 got a rare public chastisement from Bill Dembski in the comment section, he said, “Be careful, Sal.” On second thought, maybe I shouldn’t have been so careful. Even though I didn’t know much then and still don’t know much today, here is a related development 5 years after my prediction in Nature News:

Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. On average, 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. ‘There’s so many of [variants] that exist that some of them have to contribute to disease,’ says Akey

So if my prediction bears out observationally, then this debate will be closer to being settled. No need for a protracted internet war. We’ll let good old observation, hypothesis and testing settle the issue as to which side is closer to the truth.

HT JoeCoder x10
r/creation

[Thank you UD commenters for all criticisms and suggestion in improving my essays which will be archived, revised and re-expressed in various ways at CEU. I will be speaking tonight at JMU and referring students to the CEU website, and although the website is not yet the educational resource that is envisioned, maybe by next year it will have the depth I envisioned. I cross posted this draft at CEU IDCS Larry almost got it right, but he just can’t turn the corner]

Comments
Prediction by me in January 2007 (as stated in OP)
I’ve predicted rise in Single Nucleotide Polymorphisms in conserved regions since January 2007
Well, not just SNPs but entire regions! :shock: 2012
Consistent with redundant, contextual, or subtle functions, the deletion of large and highly conserved genomic segments sometimes has no discernible organismal phenotype (21, 22), and seemingly debilitating mutations in genes thought to be indispensible have been found in the human population (41). http://www.pnas.org/content/early/2014/04/23/1318948111.long
This doesn't directly prove unabated rise of SNPs as I predicted in 2007, but it certainly supports it.scordova
April 24, 2014
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Jerry @ 65
Still, the courses at Berkeley on evolution are very useful for assessing what is known about evolution. A systems biologist knows almost nothing about evolution.
When doing systems analysis, I don't care much about things that have a speculative nature, like the whole evolution-related discussion, which is interesting in itself, but not practical for writing tech specs for software development, at least in the areas I'm interested in. When writing programming specs, one tries as much as possible to stay away from ambiguities and vague concepts. Rather, one tries to describe processes, logical paths, directions, with as much certainty and clarity as possible. Let's remember that when we are trying to describe logical situations like "if 'this happens' then 'do that' else..." if the condition 'this happens' has some degree of ambiguity and vagueness, then it is more difficult to express it in a programming language. The analyst tries to write as precisely as possible, so that the programmers don't have to scratch their heads trying to figure out what to do when writing the code. The code writing process should be more a straightforward conversion of the analyst's tech specs to a language understood by the computer. That's my way of looking at this issue, on the basis of experience. Again, I'm interested in understanding the basic mechanisms behind the cell fate determination that occurs during the first weeks of human embryonic development. This refers to both functional (differentiation) and positional (migration) of the cells from the zygote on. There’s quite a bit of information on this particular subject online, but I haven’t been capable of putting all that information together into a coherent understandable description of the above mentioned events. Also interested in understanding the basic mechanisms behind the genotype-phenotype association. Again, much has been written on this subject lately, but I’m not able yet to put together all the available information into a comprehensive coherent document that could be used to write the programming specs. The discussions in this blog are quite interesting sometimes, but I want to move on with my projects. The information I'm looking for has to be mined from highly specialized technical sources. This blog does not belong to that category, though I plan to keep coming back every now and then, to look at some interesting discussions. I see this current polite discussion between you and gpuccio, with some insights from wd400 and others, as a good model of serious debate between people interested in a particular subject. We all learn a thing or two from respectful discussions like this.Dionisio
April 21, 2014
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Jerry @ 65 Khan doesn't have what I've been looking for:
interested in understanding the basic mechanisms behind the cell fate determination that occurs during the first weeks of human embryonic development. This refers to both functional (differentiation) and positional (migration) of the cells from the zygote on. There’s quite a bit of information on this particular subject online, but I haven’t been capable of putting all that information together into a coherent understandable description of the above mentioned events. Also interested in understanding the basic mechanisms behind the genotype-phenotype association. Again, much has been written on this subject lately, but I’m not able yet to put together all the available information into a comprehensive coherent document that could be used to write the programming specs.
Dionisio
April 20, 2014
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wd400: The question as to why strongly conserved regions be removed with no obvious ill effects is indeed interesting. If had to bet I’d guess at least some of it has to do with the strangeness of lab mice and lab environments. When the experimenter presented his results to the attendees of the conference, all population geneticists, biologists, etc, there was an "audible gasp." How often does that happen? And yet you show no curiosity, and simply attribute it to the "strangeness of lab rats"? Really? Basic tenets of population genetics are completely overthrown, and that's your reaction? Surely you've thought about it a little bit more and have more to say about it, right?PaV
April 20, 2014
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Saw some of their videos. Interesting pedagogical style.
Yes they are and they have been very successful. Schools all over the world are accessing his videos. But if you are interested in systems biology, they will be too basic. I thought you were just learning biology. Khan's approach is unique and great for someone just starting or wanting to brush up on a topic but not the ultimate way to delve deeply into anything. If you want to know the basics of cellular respiration, go to Khan. If you want to know the technical details of cellular respiration, a much more advanced approach is needed. Still, the courses at Berkeley on evolution are very useful for assessing what is known about evolution. A systems biologist knows almost nothing about evolution. Happy Easter from a very sunny but cool Northeast.jerry
April 20, 2014
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scordova @ 52
Can you tell us a little more about yourself and your background. Are you a student of science, and how did you find Uncommon Descent?
Electrical Engineer. Worked for a number of years on software development for engineering design (2D/3D) applications. After reading about the elaborate biological choreographies and orchestrations at cellular and molecular levels, my mind could not rest, constantly thinking about those things I had read. Gradually I realized that everything I had worked on until that point seemed relatively much simpler and even boring. I lost my interest in what I was doing. My brain was spinning around at high speed. What started as a curiosity, turned into fascination, which eventually became an obsession. After praying much about it, consulting with others, discussing with my wife and friends, I believed that God had given me this irresistible desire to start a new career path. It was a difficult decision, that caused some unpleasant arguments with some close relatives, friends and colleagues who did not understand my decision and even were against it. Perhaps some thought I was insane. Currently studying on my own (autodidact) certain aspects of systems biology associated with the processing of complex specified purpose-oriented functional information that allegedly takes place within the biological systems at the cellular and molecular levels. Working on a software development project for interactive science education, including 4D modeling and simulation. At this point particularly interested in understanding the basic mechanisms behind the cell fate determination that occurs during the first weeks of human embryonic development. This refers to both functional (differentiation) and positional (migration) of the cells from the zygote on. There's quite a bit of information on this particular subject online, but I haven't been capable of putting all that information together into a coherent understandable description of the above mentioned events. Also interested in understanding the basic mechanisms behind the genotype-phenotype association. Again, much has been written on this subject lately, but I'm not able yet to put together all the available information into a comprehensive coherent document that could be used to write the programming specs. Perhaps eventually I would like to find a scientist interested in working on this project as an advising (potential business?) partner. At this point that's just wishful thinking on the back burner of my mind. Need to pray more about this. Also working on a Christian apologetics book. I could provide more details via email or on the phone upon your request. Thank you. Happy Easter!Dionisio
April 20, 2014
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gpuccio @ 60 Wow! Those links seem like very interesting sources of information. Mile grazie!Dionisio
April 19, 2014
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jerry @ 58 Thank you for the information and suggestions. Saw some of their videos. Interesting pedagogical style.Dionisio
April 19, 2014
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scordova @ 52 My email: ------- [edited to protect commenter privacy]Dionisio
April 19, 2014
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Dionisio: As you are interested in the modeling of biological processes, I think you may be interested in the following paper from Stanford: http://www.cell.com/abstract/S0092-8674(12)00776-3 and in the corresponding web site: https://wholecell.stanford.edu/ I know that you are more interested in development of multicellular organisms, but probably you should start with simpler realities, like the prokaryotes. For metazoa, the biggest source of detailed information is probably C. elegans. You could look here: http://www.wormbook.org/ especially the "Developmental control" section. Finally, I would recommend the recent paper about Drosophila transcriptome: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12962.html Have a good time! :)gpuccio
April 19, 2014
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jerry: OK, I think we agree, more or less :)gpuccio
April 19, 2014
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Dionisio, Another source I highly recommend if you are new to biology and especially the role of DNA is the Khan Academy run by Salman Khan. This is an internet based learning site and when I went through the biology videos I was much better grounded in a lot of the basic concepts. The Khan Academy has grown like a wild fire in the last 5 years from an obscure site with the interesting videos to one of the premier internet educational sites in the world. Many schools around the world link to it for their students. Here is the link: https://www.khanacademy.org/ It wants you to sign in but ignore that and go to the bottom of the page and browse the library. If you click that you will find a list of courses and under science is biology. Click that and start with the second topic which is cells and cell division. Skip evolution because it is the politically correct version and of no use. The videos are straightforward and they err on the simple side. But some of the courses are at a very high level. Math starts out with basic 3rd grade arithmetic for the 8 year old and you can progress to Differential equations and Linear Algebra for the graduate student in college.jerry
April 19, 2014
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I am surprised that you think that I meant descent without design intervention.
I never thought that. In fact I think you believe in more design interventions than I do. I believe we should credit natural processes more than a lot here. Why, because someone with incredible intelligence designed it that way. So I believe micro evolution is a design process but it is definitely limited. And that limitation was probably a design feature but it does allow populations to adapt to changing environments. But what I have observed over the 15 years that I have been involved in this is that all non-ID persons who espouses UCD assume there was no intervention directly. So when they say they believe in UCD, they mean one where it all happened naturally. So I think the concept of UCD is a meaningless discussion because you cannot get people to agree on just what it is. And also it may not have happened even under your restricted definition. Some actually believe life started multiple times. When Elizabeth Liddle was here and she said that UCD was obvious, she was not allowing for a UCD where by an intelligence was involved. She was trying to use it as an argument against ID. And as for Behe, I believe he is keeping his cards close to the vest. One statement he said that I completely agree with and I do not know the reference is that when referring to evolution, he said "It is a mystery."jerry
April 19, 2014
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jerry: "If it means that each species uses part of a previous species" Yes. That is what it means for me. Nothing else. it means that the designer acts physically on an existing species to engineer a new species. Obviously, that can be done in different ways, in different time modalities. That remains open. The simple fact is that all the facts that darwinists invoke as evidence of "evolution" (whatever it means) are simply evidence of CD in this strict sense. So, if we accept CD in this sense, they are really left with nothing. I am surprised that you think that I meant descent without design intervention. I have always been very clear that no new complex information can be generated without an active design intervention, least of all a new species. I believe that all those in ID who accept CD (like VJ, Behe, and many others) intend in any case some form of CD through a design intervention. Otherwise, they would not be IDists. Common design is different. In that case, the designer is supposed to build the new species "from scratch", and not using an already existing species. In that case, the homologies between proteins (and other components) between species can only be explained by functional constraints, which force the designer to use similar solutions each time. But I don't like that explanation. It is not supported by facts, IMO. The problem of "universal" CD again, for me, is not probably what it is for you. First of all, I have no idea if CD is universal or not, although I tend to think it is. Second, it just means that the process that I have described started with the first designed beings (which were necessarily engineered "from scratch", and went on in all cases through new acts of design intervening on what was already done. I don't see how that would cause problems. It just means that design starts once and then goes on, that it does not start from scratch many different times. So, all living things descend from LUCA (the original prokaryote) through continuous acts of new design. What is so terrible in that? It explains very well why about half of the protein families that we find in all living beings, including humans, were already present in LUCA, the first prokaryote, and why those proteins still maintain some clear homology with human proteins, after billions of years. All those who participate in this debate usually recognize that the issue of CD is completely separate from the issue of design. That is incompatible with your statement that: "UCD means that when each organism appeared in this world, it resulted from a reproduction event of a parent or parents and nothing else." I think that is not the meaning of CD, universal or not, not only for me, but for most people who debate here. Anyway, if that is the meaning you give to the term, then obviously I don't accept that form of "common descent". I hope that is clear.gpuccio
April 19, 2014
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I gave indirect one right here:
Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. On average, 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. ‘There’s so many of [variants] that exist that some of them have to contribute to disease,’ says Akey
I have the actual paper on which the Nature article is based. It is very technical and hard to understand because of the technical terms used in population genetics. I am not sure it is saying what you are implying. There seems to be billions of healthy genomes out there but there are also a lot of unhealthy ones in one or two areas and this seems to be a cause of much disease. (Of course we are all going to die so in that way every genome is unhealthy.) I did not get any dooms day scenario from the authors. But I could be missing something.jerry
April 19, 2014
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but only after taking some online biology classes provided by some universities.
This is a good idea. There are also courses on evolutionary biology that are free. One place is the University of California at Berkeley. Each semester there two introductory biology courses are online and free. You can take courses from previous years. What you are getting is the actual lectures. It is best to supplement it with reading. http://webcast.berkeley.edu/series.html#c,d,Biology Over the years I have watched several of these courses even though they are supposedly on the same thing. When a different professor gives the course you get a different perspective. There is nothing in the evolution part of these courses that refutes ID. I found that very interesting and if Berkeley cannot present evidence for natural evolution, then no one can. The best way to learn evolution is to read and watch what the opponents of ID say. Not once have I ever saw anything from these people that refutes ID.jerry
April 19, 2014
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gpuccio, We are really dealing with semantics here. What does the term CD (common descent) and UCD (universal common descent) mean. If it means that each species uses part of a previous species then I will give you your definition of the term. But it also means there was only one parent or set of parents that started this process. However, it has come to mean much more than this. UCD means that when each organism appeared in this world, it resulted from a reproduction event of a parent or parents and nothing else. There is no insertion of information from an outside source to change the nature of the offspring and whatever change in information that happened within the parent(s) took place as a result of natural forces. Now ID could say that these natural forces were manipulated somehow either by boundary conditions or by manipulation of exogenous forces by something like a quantum event. (some of the TE's believe this is the way change happened and how God operates. He influences the roll of the dice.) However, the evidence to date indicates that the changes were massive and not subtle. Otherwise the quantum changes would leave a forensic trail just as random mutation would leave a trail. There is no trail. But some will say that the creator obliterated the trail. Possible but why? We are into another conundrum. Unless we accept the hopeful monster scenario we are left with a source outside the parent organism as a major source of the information and the parent is only a convenient vehicle for the instantiation of the new information which came from another source. If you want to call that UCD then ok. But I do not consider that UCD. And in the specific case when the information is inserted, I do not consider it CD. So using the common definition (Universal common descent through an evolutionary process, that there was only one progenitor for all life forms, was first proposed by Charles Darwin in On the Origin of Species,) we have the word progenitor. But the offspring is not descendant from the parent when an intelligent agent interferes with the new organism. Part or nearly all of the offspring is independent of the parent(s). So if a progenitor is involved it is something other than the parent organism. (Is the intelligence one of the parents?) If you want to say that the intelligence is the same in each case then I guess you can say that there is UCD. It all came from this intelligence. Then your understanding of the progenitor is quite different from what others hold. I prefer to make the distinction and say that when an insertion of information from an outside intelligence is made, that the offspring is not a common descendant of its biological parent(s). We are now or almost capable of creating new life forms from scratch. If we can do it, why not some other intelligence. And if we use most of the current coding sequences to do so, is the new organism an example of UCD. I think not. Anyway it not a big issue of difference between us but if one says that they support UCD then there is a lot of baggage that is assumed to come with it. I take the point of view that there is no evidence to say there was an unbroken line. The Cambrian is such a break in the line. There are others.jerry
April 19, 2014
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Dionisio, Can you tell us a little more about yourself and your background. Are you a student of science, and how did you find Uncommon Descent?scordova
April 19, 2014
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Correction to #50
much much many more visitors...
Dionisio
April 19, 2014
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OT: After reading the comments in this thread, specially the interesting discussion between gpuccio and jerry, I'm starting to get a very elementary idea of some of the discussed subjects. This confirms that for those of us who come from engineering software development professions and are trying to work in the growing biological field, some of these threads could be partially used as complementary tools for learning certain aspects of biology, but only after taking some online biology classes provided by some universities. Some of my previous comments in this thread referred to terminology issues related to the use of words that could turn controversial and confusing to the new 'guests' in the 'party' ;-) If we have two interchangeable terms, but one could be more controversial and confusing than the other, then why not use the less controversial term? That was all. Now, after reading gpuccio's explanation, I started to better understand why some terms are used and their contextual significance. Thank you gpuccio! Just wanted to share this personal learning experience with y'all, so you know the influence your posts and follow-up comments can have on visitors to this blog. There are much much more visitors (i.e. readers) than commentators (i.e. writers) in this blog, at least according to the statistics provided at the end of each OP. At this point my interest is focused in on the cell fate determination mechanisms that work during the first weeks of human development from the zygote on. There's much information on that subject online. It would be interesting to see some discussions on this subject in this blog too. From a 4D in-silico modeling/simulation perspective, this subject presents some interesting challenges. Thank you all. Enjoy the weekend.Dionisio
April 19, 2014
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jerry: I have no doubts that you are a design supporter. But, as you often mention, with the due respect, specific naturalist arguments, I try to explain to you why I am not impressed by them. That's all. I wholly agree with most of what you write in you post. I beg to explicitly differ on two points, the first one important, the second not too much: 1) You say:
When such an insertion takes place, I maintain that is a break in common descent.
And I simply ask: why? An insertion of information (which, like you, I believe happened a lot of times, indeed probably more often than you believe, see point two) is not in itself a "break in common descent. I absolutely believe in the active insertion of information at definite times, and still I fully accep CD as the best explanation for some aspects of what we observe (as I have detailed many times). Let's be more clear. a) We have species A, with sequence a (let's say it is a non coding sequence). b) At some specific time, species B, with functional sequenc e b (let's say it's a protein coding gene) appears. Now, I am not saying, in any way, that b explains B. b is just useful to B, but probably B needs a lot of other things to appear (new regulatory procedures, wherever they are written, a new body form, wherever it is written, and so on). I have no idea if these other things are derived from something which was already present in A, or not. Unless and until we can detail their molecular basis, nobody can tell. c) But I know one thing, because I can see it in my molecular results: a and b, while different, present striking sequence homologies, well beyond what can be explained by chance. Let's say that, if I blast the two sequences one vs the other, I get a e value of 1e-90. That means that there is one probability out of 10^90 to get that similarity by chance in the whole sequence database I am looking at. Now, that is exactly the kind of thing which requires some explanation. That's exactly the kind of thing on which we base the whole of ID theory. So, I cannot underestimate it. I must provide an explanation. And the best explanation is: a was prepared by a designer in A, or even before, to become b at the time the new species was designed to arise. IOWs, there are two alternatives: a) b was generated from scratch at the time that species B arose. But then, why is it so similar to a? b) the designer designed B not from scratch, but rather intervening on A and physically reusing part of what A was, and modifying, adding or deleting whatever he considered necessary. Therefore, b is similar to a because a was physically used to build b. I choose the second explanation, because for me it's the only one which makes sense. If I could believe that a sequence is similar to another one out of chance, with a 1e-90 probability of that event, I could as well become a darwinist! :) And please, not that common design cannot be invoked in this scenario, because a is not an ORF in species A, so there is no functional need for it to be similar to b, an ORF which will appear in the future. The only reason for that is that it will be used in the future to build that ORF. I hope the point is clear enough. 2) Of minor importance: I am not sure I agree with you about beetles. I have not studied the problem in detail, but my approach would simply be: if beetle species, however numerous, differ one from the other for important functional traits, like new functional proteins, then I would infer design anyway. But, if they differ only for a few bits of functional information, then they can well be ascribed to random variation, with or without NS. But frankly, the evolution of beetle species is not one of my priorities, for now :)gpuccio
April 18, 2014
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gpuccio,
Do you really believe that we can understand anything of that, without reasoning in terms of design and purpose?
You seem to be implying that I am somehow questioning ID. I doubt that there is any bigger supporter of ID here on this site. But I am only interested in what is true because to push something that is untrue leads others away and not toward. So I question a lot of things and tend to tentatively hold things that I believe make the most sense. I keep on changing what I believe happened as more information becomes available. You will never see me defending common descent in terms of UCD because the evidence points away from it. I will take the position that I know of no mechanism other than intelligence that could account for certain changes in life. Meyer takes the same position that there must be insertions of information at various times to account for what happened. When such an insertion takes place, I maintain that is a break in common descent. But I don't think it is important when and how the information was inserted. It just had to be inserted. I tend to support that a lot of change happened naturally and not due to a continual insertion of small changes by a designer but these can only be small changes. I essentially believe Behe destroyed the viability of naturalistic processes for anything major. For example, do I believe that some intelligence was responsible for all the species of beetles. Definitely not. What I believe is that the machinery of the cell has been designed to provide variety and mutations help with this variety but only to a certain extent. There are definitely very defined limits on how a population can change over time but they definitely can change due to the environment. Ray Bohlin wrote one of the best books on this, The Natural Limits to Biological Change. It was one of the first things I read about 15 years ago. The naturalists have no credible system for the origin of new genes that produce truly unique proteins. We are only now mapping large number of genomes. The price in money and time gets lower every year. You can get part of a human genome for about $15. And these could be made larger to answer some of the questions about conserved regions from populations around the world. I proposed the comparison of European, African and Australian natives. That should be easy to do with universities from each continent collecting the data. Maybe add some South American natives and some from various places in Asia. A lot of this DNA is available from previous studies so could be compared. Also there is DNA from humans of several thousand years ago that has been found and supposedly there is Neanderthal DNA. We would answer a lot of questions about what is essential in the genome of humans from data already collected.jerry
April 18, 2014
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The question as to why strongly conserved regions be removed with no obvious ill effects is indeed interesting. If had to bet I'd guess at least some of it has to do with the strangeness of lab mice and lab environments. But, with regards the wider point - there is abundant evidence to the operation of purifying selection in modern genomes, in coding and some non-coding regions.wd400
April 18, 2014
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An airline tried to figure out what parts of their passenger aircraft were non-functional, so the airline could cut their costs by removing the unnecessary parts in order to reduce the aircraft weight and burn less fuel. They hired this company Nocose to write a report. The Nocose experts looked inside and outside the aircraft. They noticed some flat dark rectangular objects on the back of the seats in the economy class. Since they had no idea what they were for, they requested a test. So the maintenance technicians removed the flat rectangular objects and had the plane take off. They monitored a number of sensors they had placed in different parts of the aircraft. At the end of the test flight, the Nocose experts concluded that since no major problem had been detected in the test flight, the removed objects had no beneficial function, therefore they could be removed. Well, the airline followed the suggestion and removed the same objects from all the planes in their fleet. Sometime later, after noticing that most passengers were flying with the competition, they hired another company named Cose to figure out the reason for the passengers choosing the competition for their traveling. The hired contractors simply asked a random sample of passengers at the airport. Curiously their responses were all the same: the competition shows movies, games, news, etc. on small screens they have on the back of their seats in the economy class. [note: Nocose stands for no common sense] Is it possible similar situations could occur in other areas of human activities?Dionisio
April 18, 2014
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conservation should be linked to function.
Yes, that is a God-given road map to help scientists learn biology. It is steganography not conservation in sequences as Bill said:
Steganography Finally, we come to the research theme that I find most intriguing. Steganography, if you look in the dictionary, is an archaism that was subsequently replaced by the term “cryptography.” Steganography literally means “covered writing.” With the rise of digital computing, however, the term has taken on a new life. Steganography belongs to the field of digital data embedding technologies (DDET), which also include information hiding, steganalysis, watermarking, embedded data extraction, and digital data forensics. Steganography seeks efficient (that is, high data rate) and robust (that is, insensitive to common distortions) algorithms that can embed a high volume of hidden message bits within a cover message (typically imagery, video, or audio) without their presence being detected. Conversely, steganalysis seeks statistical tests that will detect the presence of steganography in a cover message. Consider now the following possibility: What if organisms instantiate designs that have no functional significance but that nonetheless give biological investigators insight into functional aspects of organisms. Such second-order designs would serve essentially as an “operating manual,” of no use to the organism as such but of use to scientists investigating the organism. Granted, this is a speculative possibility, but there are some preliminary results from the bioinformatics literature that bear it out in relation to the protein-folding problem (such second-order designs appear to be embedded not in a single genome but in a database of homologous genomes from related organisms). While it makes perfect sense for a designer to throw in an “operating manual” (much as automobile manufacturers include operating manuals with the cars they make), this possibility makes no sense for blind material mechanisms, which cannot anticipate scientific investigators. Research in this area would consist in constructing statistical tests to detect such second-order designs (in other words, steganalysis). Should such second order designs be discovered, the next step would be to seek algorithms for embedding these second-order designs in the organisms. My suspicion is that biological systems do steganography much better than we, and that steganographers will learn a thing or two from biology — though not because natural selection is so clever, but because the designer of these systems is so adept at steganography. Such second-order steganography would, in my view, provide decisive confirmation for ID. Yet even if it doesn’t pan out, first-order steganography (i.e., the embedding of functional information useful to the organism rather than to a scientific investigator) could also provide strong evidence for ID. For years now evolutionary biologists have told us that the bulk of genomes is junk and that this is due to the sloppiness of the evolutionary process. That is now changing. For instance, Amy Pasquenelli at UCSD, in commenting on long stretches of seemingly barren DNA sequences, asks us to reconsider the contents of such junk DNA sequences in the light of recent reports that a new class of non-coding RNA genes are scattered, perhaps densely, throughout these animal genomes. (microRNAs: Deviants no Longer. Trends in Genetics 18(4) (4 April 2002): 171-3.) ID theorists should be at the forefront in unpacking the information contained within biological systems. If these systems are designed, we can expect the information to be densely packed and multi-layered (save where natural forces have attenuated the information). Dense, multi-layered embedding of information is a prediction of ID. It’s time to bring this talk to an end. I close with two images (both from biology) and a final quote. The images describe two perspectives on how the scientific debate over intelligent design is likely to play out in the coming years. From the vantage of the scientific establishment, intelligent design is in the position of a mouse trying to move an elephant by nibbling at its toes. From time to time the elephant may shift its feet, but nothing like real movement or a fundamental change is about to happen. Let me emphasize that this is the perspective of the scientific establishment. Yet even adopting this perspective, the scientific establishment seems strangely uncomfortable. The mouse has yet to be squashed, and the elephant (as in the cartoons) has become frightened and seems ready to stampede in a panic. The image that I think more accurately captures how the debate will play out is, ironically, an evolutionary competition where two organisms vie to dominate an ecological niche (think of mammals displacing the dinosaurs). At some point, one of the organisms gains a crucial advantage. This enables it to outcompete the other. The one thrives, the other dwindles. However wrong Darwin might have been about selection and competition being the driving force behind biological evolution, these factors certainly play a crucial role in scientific progress. It’s up to ID proponents to demonstrate a few incontrovertible instances where design is uniquely fruitful for biology. Scientists without an inordinate attachment to Darwinian evolution (and there are many, though this fact is not widely advertised) will be only too happy to shift their allegiance if they think that intelligent design is where the interesting problems in biology lie. https://uncommondescent.com/intelligent-design/how-idists-can-win-the-war/
scordova
April 18, 2014
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If the deletion has not discernible phenotypic effect is hard to see what’s being lost.
If deletions have no discernible phenotypic effect, then why should it be "conserved" in the first place? Maybe it isn't conserved, maybe it was intelligently designed to be similar at first and now it is slowly deteriorating. We might not detect the deterioration if we aren't looking for it. That is my point. gpuccio pointed out:
(UCEs or UCRs) that share 100% identity among human, mouse and rat were first described by Bejerano and colleagues in 2004.[1] One recent study that eliminated four highly-conserved non-coding DNA sequences in mice yielded viable mice with no significant phenotypic differences; the authors described their findings as “unexpected"
Of course it's unexpected because it violates the presumption "conserved" sequences are under selection. And if the presumption the conserved sequences are under selection is violated, it may mean they aren't under selection, and if they aren't under selection, they may not be conserved in the first place but specially created and deteriorating slowly thereafter, exactly the ReMine/Sanford Neutral model (special creation followed by nearly neutral evolution). The good news is unlike other topics in the origins debate that might never have resolution, we will be getting more data in the future. We will know if the "conserved" regions are really conserved, or whether the are slowly getting scrambled in real time. If gametic mutation rates are 10^-8 per bp per generation and if we can be lucky enough to find 10^6 UCE base pairs: 10^8 * 10^6 = 10^-2 So if we sample 10^4 individuals we might be able to get 10^2 mutants per generation in 10^4 individuals. Are our lab methods error-free enough to detect such a change? Any way, I shouldn't be monkeying with this stuff. Guys like Eyre-Walker and Keithley and Nachman and Crowell and Michael Lynch and others should be doing this. They've got the brains and background, not me. I just report on the issues and point out the mice knockout experiments are a serious issue.scordova
April 18, 2014
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jerry: I agree with you. In general, conservation should be linked to function. If that is the case, a lot of non coding DNA should be functional. The mice experiment cited in Wikipedia has been criticized, but still it is part of the few data we have on this issue. I think that function can have many aspects. One of the deformations of thought induced by neo darwinism is that we tend to think of function mainly as reproductive success or just survival. But I believe that there is much more to it. It is very true that we still don't understand regulatory functions. So, we look at those huge oceans of repetitive sequences, and wonder: what can they really do? But they can do things. We already know many of those things, and many more will come. I believe that all the fashionable trend about epigenetics, while interesting, can be misleading. Let's take humans, for example. They have a brain which is much more complex, and more functional, than the brain in primates. And yet we find not too much "novelty", apparently, at the genome level. So, we say: it's epigenetic, it's regulatory. But we must understand what it means. Regulations depend on procedures. And procedures, unles we believe that they arise spontaneously from nothing, must be written somehwere. Procedures are transmitted. All humans have brains with similar structures and functions. And all chimps have brains with less developed structures and functions. There must be a reason for that. And that reason must be transmittable. OK, part of it could not be in the genome proper. Part of it could be transmitted by the cytoplasm of the egg cell. But I think that it is perfectly reasonable to believe that most of it must be in the genome. After all, regulatory RNAs, which are the main actors in what we know of regulations, are transcribed from DNA. From the whole genome, including introns and interspersed repetitive elements. Transcription factors are proteins. They are syntetised from the genome. Regulatory peptides come from the genome. Methylations are epigenetic, but what determines the pattern of methylation? So, in the end, we must understand how the genome works. Or, even better, how the integrated unity which is the genome plus the other nuclear components (RNAs, etc), plus the cytoplasmic components, work as a complex whole. Do you really believe that we can understand anything of that, without reasoning in terms of design and purpose?gpuccio
April 18, 2014
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I would say that we still need more information to fully understand which regions of the genome are conserved across species, and why.
Thank you. I read the Wikipedia stuff on this the last couple days but cursorily. Things like your post on this should be in a resource part on this site so we can access it when a question comes up about it. I have a hard time understanding why a region can be conserved, essentially exempt from mutation, and not be functional. What is preventing the mutations?jerry
April 18, 2014
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I'm not sure you've really though this through. Expanding population is given as the excuse for the absence of selection, but even granting that, it still proves absence of selection implies deterioration Expanding population is the reason for an excess of rare variants. Selection is still evident among those rare variants. In fact Figure 3 in the first paper(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708544/#!po=57.6923), and discussion there-abouts in entirely about the effect of purifying selection in these sites. ook those knockout experiments with mice. Deeply conserved in both humans and mice 100%. Did the mice die? No. Did it have noticeable effect? No. Ergo it’s probably not under selection, ergo it could be deteriorating What's deteriorating? If the deletion has not discernible phenotypic effect is hard to see what's being lost.wd400
April 18, 2014
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This fundamental conflict is evidence to me that both Darwinism (and its materialistic successors) and ID are paradigms, not theories.
Querius, I am in agreement with you on this perspective. Science and mathematics can inform us about these paradigms, as you have characterized them, but they are not themselves science. Since the events covered by the paradigms are all in the remote past, there is no testability, direct observation or repeatability within those paradigms. Most, all?, of what we "know" of these paradigms is inaccessable to anything that could be described as a scientific methodology. StephenSteRusJon
April 18, 2014
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