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Double debunking: Glenn Williamson on human-chimp DNA similarity and genes unique to human beings

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Computer programmer Glenn Williamson now claims that ICR geneticist Jeff Tomkins made an elementary error when using the nucmer program to show that human and chimp DNA are only 88% similar. Williamson also asserts that 60 de novo protein coding genes said to be unique to human beings have very similar counterparts in apes, contrary to claims made last year by Dr. Cornelius Hunter, who is an adjunct professor of biophysics at Biola University.

What Dr. Tomkins allegedly got wrong

As readers of my recent post, Human and chimp DNA: They really are about 98% similar, will recall, Glenn Williamson demolished Dr. Tomkins’s original claim, made back in 2013, that human and chimp DNA are only about 70% similar. Williamson’s detailed takedown of Dr. Tomkins’s 70% similarity figure can be accessed here. In short: the version of the BLAST computer algorithm used by Tomkins contained a bug which invalidated his results. Dr. Tomkins responded by performing a new study which came up with a similarity figure of 88% – still far below the 98% similarity figure commonly claimed in textbooks for human and chimp DNA. Tomkins arrived at that figure by using a version of the BLAST algorithm which did not contain the bug, and in my last post, I pointed out the errors identified by Glenn Williamson in Dr. Tomkins’ new paper, relating to BLAST.

But to give credit where credit is due, Dr. Tomkins didn’t rely on just one computer program to come up with his 88% figure; he relied on three. In addition to BLAST, Dr. Tomkins made use of two other programs: nucmer and LASTZ. Creation scientist Jay Wile described these programs in a recent post discussing Dr. Tomkins’ work:

The nucmer program’s results agreed with the unbugged BLAST results: on average the human and chimpanzee genomes are 88% similar. The LASTZ program produced a lower average similarity (73%), which indicates that perhaps LASTZ has a bug or is not optimized for such comparisons, since its results are very close to the results Dr. Tomkins got with the bugged version of BLAST.

In today’s post, I’ll discuss the flaws identified by Glenn Williamson in Dr. Tomkins’s comparisons that were made using the nucmer program.

Basic methodological errors?

As we saw in yesterday’s post on Uncommon Descent, Glenn Williamson claims that Dr. Tomkins’s new study makes some fundamental errors in the way it performs the BLASTN analysis. Now, however, Williamson has gone further, and identified some very basic errors in the way Dr. Tomkins obtained his results from the nucmer program. What Williamson has shown is that even when human chromosome 20 is compared with itself, the calculation method used by Dr. Tomkins when running the “nucmer” program would imply (absurdly) that it is less than 90% similar to itself!

I have been in email correspondence with Glenn Williamson over the past 24 hours, and he kindly allowed me to publish his responses, as well as some emails he sent to Dr. Tomkins. Here’s an excerpt from his first email to me.

Hi Vincent,

I’ve only just seen your post on UD, and I thought I’d fill you in on where we are at with one of the other comparisons (“nucmer”) Jeff did in his recent paper. Basically what he is doing in this comparison is taking every single alignment for each query sequence (as opposed to taking just the best alignment) and taking the average of all those. Obviously all the repeat motifs will find many matches across each chromosome, but only one of those will be (putatively) homologous. If you can follow the email thread from the bottom, hopefully you can understand the issue.

I’m currently running a nucmer job with human chromosome 20 being compared to itself, just to show the absurdity of his calculation method. I should have the results by tomorrow.

I subsequently emailed him, and asked if he could tell me about the results:

I would greatly appreciate it if you would let me know about your results, after you finish running your nucmer job. I was also wondering if you would allow me to quote excepts from your correspondence in a forthcoming post on UD.

Glenn Williamson replied:

Hey,

Yup, no problems quoting any of the emails…

The first nucmer job I ran took 37 hours (human 20 to chimp 20), and this current “control” job (human 20 to human 20) has taken 37 hours as of right now, so it should finish soon. It will take a couple of hours to put all the results together, so should have something by tonight.

It wasn’t long before I heard from Glenn Williamson again:

It’s done!

And human chromosome 20 is only 88.86% identical to human chromosome 20! 🙂

Unix commands, if you care:

awk ‘NR>5 { print $7″\t”$8″\t”$10 }’ control.coords > control.tab
awk ‘{ sum += ($1 + $2) / 2; prod += ($1 + $2) / 2 * $3 } END { print prod; print sum; print prod / sum }’ control.tab

Output:

1.71549e+09
1.52439e+11
88.8601

So basically the alignments covered 1.715Gb for a chromosome that is only 64Mb long (27x coverage). There were 4.8 million individual alignments …

So there we have it. If Dr. Tomkins is right, then not only is chimpanzee DNA only 88% similar to our own, but human DNA is only 89% similar to itself!

Do human beings really have 60 de novo protein-coding genes with no counterparts in apes?

But there was more – much more. In my original email to Glenn Williamson, I had expressed curiosity over a comment he made on a January 2014 post titled, Chinese Researchers Demolish Evolutionary Pseudo-Science, over at Dr. Cornelius Hunter’s Website, Darwin’s God, in which Williamson expressed skepticism over Dr. Hunter’s claim that no less than 60 protein-coding orphan genes had been identified in human DNA which had no counterpart in chimpanzees. To support his claim, Dr. Hunter cited a 2011 PLOS study by Dong-Dong Wu, David M. Irwin and Ya-Ping Zhang, titled De Novo Origin of Human Protein-Coding Genes. Here is the authors’ summary of their paper (emphases mine – VJT):

The origin of genes can involve mechanisms such as gene duplication, exon shuffling, retroposition, mobile elements, lateral gene transfer, gene fusion/fission, and de novo origination. However, de novo origin, which means genes originate from a non-coding DNA region, is considered to be a very rare occurrence. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee, supported by both transcriptional and proteomic evidence. It is inconsistent with the traditional view that the de novo origin of new genes is rare. RNA–seq data indicate that these de novo originated genes have their highest expression in the cerebral cortex and testes, suggesting these genes may contribute to phenotypic traits that are unique to humans, such as development of cognitive ability. Therefore, the importance of de novo origination needs greater appreciation.

Commenting on the paper, Dr. Hunter remarked (bold emphases mine – VJT):

A 2011 paper out of China and Canada, for example, found 60 protein-coding genes in humans that are not in the chimp. And that was an extremely conservative estimate. They actually found evidence for far more such genes, but used conservative filters to arrive at 60 unique genes. Not surprisingly, the research also found evidence of function, for these genes, that may be unique to humans.

If the proteins encoded by these genes are anything like most proteins, then this finding would be another major problem for evolutionary theory. Aside from rebuking the evolutionist’s view that the human-chimp genome differences must be minor, 6 million years simply would not be enough time to evolve these genes.

In fact, 6 billion years would not be enough time. The evolution of a single new protein, even by evolutionists’ incredibly optimistic assumptions, is astronomically unlikely, even given the entire age of the universe to work on the problem.

Note the claim that Dr. Hunter is making here: “60 protein-coding genes in humans that are not in the chimp.” But as we’ll see, these genes do have virtually identical counterparts in chimps, even if they are noncoding.

So, how many ORFan genes do humans really have?

In his comment, Glenn Williamson responded to Dr. Hunter’s claim that humans have 60 protein-coding genes that are “not in the chimp” by pointing out that the first of these 60-odd genes actually has a counterpart in chimpanzee DNA which is 98% identical to the human gene (emphasis mine – VJT):

“So how many ORFan genes are actually in humans???”

Depends what you call an ORFan gene. I looked at the paper that Cornelius cites as having 60 de novo protein coding genes.

Now, granted that I only looked at the very first one (“ZNF843”), it was quite easy to find the corresponding DNA on the chimpanzee chromosome, with approximately 98.5% identity.

So whether it is protein-coding in humans and non-coding in everything else doesn’t really concern me. What concerns me is whether it has an evolutionary history: clearly this one does.

Like I said, I’ve only done one. I’d happily take bets on the majority of these de novo genes having an evolutionary history (chimpanzee > 95% and/or gorilla > 90%).

Any takers?

I had only come across this exchange in the last couple of days, while surfing the Net, and my curiosity was piqued. So I wrote back to Williamson:

By the way, I was intrigued with your work on orphan genes, and I thought I’d have a look at the 60 genes mentioned by Cornelius Hunter in a post he wrote last year. However, I don’t have any experience in this area. Can you tell me how to go about running these comparisons?

Orphan genes – did Dr. Hunter get his facts wrong?

Glenn Williamson’s reply was very helpful – and it pulled no punches. He accused Dr. Hunter of getting his facts wrong about ORFan genes (emphasis mine – VJT):

As for Orphan genes, I assume you mean this comment? http://darwins-god.blogspot.com.au/2014/01/chinese-researchers-demolish.html?showComment=1421299517820#c1105680265537141676

There are a couple of points to be made here. First is that Cornelius fundamentally misunderstands what an orphan gene is and what an ORF(an) is – they are not equivalent terms. A true orphan gene should be called a “taxonomically restricted gene” (TRG), and no trace of its evolutionary history can be found outside a particular taxonomic group. These would be examples of de novo evolution. With respect to humans and chimpanzees, I don’t know of any TRGs that exist in either genome (with respect to the other), and if there were, I would then check the other great apes to see if it was likely that this gene was deleted in one of the genomes (rather than evolved out of nothing in 6mn years!).

Good point. Williamson continued:

An ORFan gene usually refers to a putative protein coding gene. “Putative” because these are generally the result of a computer program trying to find long open reading frames, and if it finds something over a certain length (300bp? 400bp?) then, since a long open reading frame is quite unlikely, the program thinks that this open reading frame is evolutionarily conserved, and it might be conserved because it codes for an important protein. Have a read of Eric Lander’s paper – http://www.ncbi.nlm.nih.gov/pubmed/18040051 – where he says we should be removing these ORFs from the gene database unless and until we can actually find their corresponding proteins.

Glad we got that point cleared up. So, what about those 60 protein-coding genes in humans which Dr. Hunter claimed are not found in the chimp? Here’s what Williamson wrote back to me:

So, these 60-odd genes that Cornelius brings up, he is claiming that they must have evolved de novo:

“In fact, 6 billion years would not be enough time. The evolution of a single new protein, even by evolutionists’ incredibly optimistic assumptions, is astronomically unlikely, even given the entire age of the universe to work on the problem.”

And that’s why I checked the first one on the list, just to demonstrate that it was in the chimpanzee genome (at 98.5% identity). So if this gene codes for a protein in humans, maybe we just haven’t found the protein in chimps. Maybe it codes for a protein in humans, and there was a single mutation that caused it not to be translated in chimps. Maybe it doesn’t actually code for a protein in humans at all? (Although I think we can check that). In any case, it’s not an example of de novo evolution – it’s not an orphan gene in the sense of being taxonomically restricted.

As to how to do the work yourself .. let me send this one off first and I’ll start another email 🙂

For my part, I am somewhat skeptical about Williamson’s speculation that these genes got switched off in the lin leading to chimpanzees – especially in view of the discovery of three undoubted cases of de novo genes in human beings where the ancestral sequence in apes was noncoding. But given the striking 98% similarities between these genes and their non-coding counterparts in apes, I would also urge caution about Dr. Hunter’s claim that even billions of years would not have been long enough for these protein-coding genes to have evolved. If they were evolving from scratch, yes; but if they were evolving from 98% identical counterparts, I wouldn’t be so sure about that.

I learn how to do a BLAST comparison

In his next email, Glenn Williamson kindly informed me how to do a BLAST comparison, and how he obtained his results for ZNF843, which was the first of the 60 de novo protein coding genes cited by Dr. Hunter in his 2014 post. In his response to Dr. Hunter, Williamson had reported that “it was quite easy to find the corresponding DNA on the chimpanzee chromosome, with approximately 98.5% identity.” Here’s what he wrote to me:

Alright, I’ll run you through a simple BLAST search on the Ensembl website. Although, if you want to do some serious BLASTing, then you probably should install the software on your own machine, and download the genomes onto your hard drive.

Anyway, go to:

http://www.ensembl.org/index.html

and stick the name of the gene: ZNF843 into the search box. That should get you to here:

http://asia.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000176723;r=16:31432593-31443160

On the left hand side, there should be an “Export Data” tab. Click it. Deselect all the checkboxes (we just want the raw DNA) and hit “Next”. Hit the “Text” button, and then just Copy the whole output, starting with the “>blah blah blah”. Now, at the top left of the page is the “BLAST/BLAT” tool. Click it.

Paste the copied DNA into the box, make sure you search against the chimpanzee genome (i.e. uncheck the human genome) and then run the search – using the default parameters should be fine for now.

The results can be found here:

http://www.ensembl.org/Homo_sapiens/Tools/Blast/Ticket?tl=mQCTv8YnFRQKB0Kx

Unfortunately the results are given in chunks, and if you want to get an exact number, stick them in Excel and work it out. But if you just want to look at it on the website, click on the “Genomic Location” header to sort them in that order, scroll down to chromosome 16, and you’ll see that it covers the vast majority of the 10.5kb of query DNA, and the matches are around 98.5%-99.5%. Rough guess for the overall identity (including some small indels) is about 98.5%.

If you need help just email me back and I’ll see what I can do. I gotta run now tho 🙂

And here’s what Williamson got when he ran the BLAST comparison on his computer:

I ran it on my local machine:

#!/bin/sh

QRY=”ZNF843.fa”
SBJ=”${HOME}/Data/Ensembl/chimp/Pan_troglodytes.CHIMP2.1.4.dna.chromosome.16.fa”

blastn -query ${QRY} -subject ${SBJ} -max_hsps 1 -outfmt ’10 qseqid qstart qend sstart send nident pident qlen length’

Output:

16,1,10568,31611859,31601307,10375,97.62,10568,10628

So, only 97.62% identity for that one … 0.57% of the alignment is indels. Boooooooooooooo.

So, for the first of the alleged 60 “de novo” protein coding genes cited by Dr. Hunter (“ZNF843″), Glenn Williamson managed to locate some corresponding DNA on the chimpanzee chromosome, which was approximately 98% identical. Are these genes without an evolutionary history? I hardly think so!

More good news – the results for all the other genes are already in!

In his most recent email, Glenn Williamson shared further good tidings: comparisons for the other 59 genes have already been done!

Just looking into that 2011 paper a little further – they’ve already done all the work for us!

http://journals.plos.org/plosgenetics/article/asset?unique&id=info:doi/10.1371/journal.pgen.1002379.s009
http://journals.plos.org/plosgenetics/article/asset?unique&id=info:doi/10.1371/journal.pgen.1002379.s011

These are the 60 “de novo” genes, and their alignments with chimpanzee and orang-utan 🙂

I’ve had a look at the output, and even to my untutored eye, it’s obvious that any claims that these “de novo” genes are not found in the DNA of chimps and other apes are flat-out wrong. They have virtually identical counterparts on the chimpanzee and orang-utan genomes, even if these are non-protein coding.

Some cautionary remarks about the 2011 paper cited by Dr. Hunter

The 2011 paper by Wu et al. which was cited by Dr. Hunter was critiqued in another article in PLOS Genetics (7(11): e1002381. doi:10.1371/journal.pgen.1002381, published 10 November 2011), titled,
De Novo Origins of Human Genes by Daniele Guerzoni and Aoife McLysaght. The authors felt that the estimate of 60 de novo human-specific genes in the paper by Wu et al. was based on rather lax criteria. What’s more, they seemed confident that the genes could have evolved:

In this issue of PLoS Genetics, Wu et al. [15] report 60 putative de novo human-specific genes. This is a lot higher than a previous, admittedly conservative, estimate of 18 such genes [13], [16]. The genes identified share broad characteristics with other reported de novo genes [13]: they are short, and all but one consist of a single exon. In other words, the genes are simple, and their evolution de novo seems plausible. The potential evolution of complex features such as intron splicing and protein domains within de novo genes remains somewhat puzzling. However, features such as proto-splice sites may pre-date novel genes [9], [17], and the appearance of protein domains by convergent evolution may be more likely than previously thought [2].

The operational definition of a de novo gene used by Wu et al. [15] means that there may be an ORF (and thus potentially a protein-coding gene) in the chimpanzee genome that is up to 80% of the length of the human gene (for about a third of the genes the chimpanzee ORF is at least 50% of the length of the human gene). This is a more lenient criterion than employed by other studies, and this may partly explain the comparatively high number of de novo genes identified. Some of these cases may be human-specific extensions of pre-existing genes, rather than entirely de novo genes — an interesting, but distinct, phenomenon.

In a 2009 paper titled Recent de novo origin of human protein-coding genes (Genome Research 2009, 19: 1752-1759), David Knowles and Aoife McLysaght presented evidence for the de novo origin of at least three human protein-coding genes since the divergence with chimp, and estimated that there may be 18 such genes in the human genome, altogether. Here’s what they said about the three genes they identified:

Each of these genes has no protein-coding homologs in any other genome, but is supported by evidence from expression and, importantly, proteomics data. The absence of these genes in chimp and macaque cannot be explained by sequencing gaps or annotation error. High-quality sequence data indicate that these loci are noncoding DNA in other primates. Furthermore, chimp, gorilla, gibbon, and macaque share the same disabling sequence difference, supporting the inference that the ancestral sequence was noncoding over the alternative possibility of parallel gene inactivation in multiple primate lineages.

Note the wording: “Each of these genes has no protein-coding homologs in any other genome.” Nevertheless, the genes have non-coding counterparts in the DNA of apes: “High-quality sequence data indicate that these loci are noncoding DNA in other primates.”

Whether these genes could have evolved naturally from their ape counterparts is a question I’ll leave for the experts to sort out. One thing I do know, however: they are not “new” in the sense that layfolk would construe that term – that is, functioning genes which have no counterparts in the DNA of apes. Clearly, they do have very similar counterparts in apes, even if those counterparts are non-coding.

Conclusion

Well, I think that’s about enough new revelations for one day, so I shall stop there. It seems to me that any claims that humans have a large number of “de novo” genes with no counterparts in the DNA of chimpanzees and other apes should be treated with extreme caution. In fact, I wouldn’t bet on our having any de novo protein-coding genes having no counterparts in apes, after that takedown.

We already have very good arguments demonstrating the impossibility of proteins having evolved via an undirected process, thanks to the excellent work of Dr. Douglas Axe – see, for instance, his excellent article, The Case Against a Darwinian Origin of Protein Folds. It seems to me that arguments based on de novo genes alleged to exist in human beings, with no counterparts in apes, have much weaker evidential support, and that Intelligent Design proponents would be better off not using them.

But perhaps those who are feeling adventurous might like to take up Glenn Williamson on his 2014 wager:

I’d happily take bets on the majority of these de novo genes having an evolutionary history (chimpanzee > 95% and/or gorilla > 90%).

Any takers?

Well? Is anyone feeling lucky?

POSTSCRIPT: Readers may be interested to know that Dr. Ann Gauger has written a very balanced post titled, Orphan Genes—A Guide for the Perplexed. In her post, Dr. Gauger defines orphan genes as ” those open reading frames that lack identifiable sequence similarity to other protein-coding genes.” Note the word “protein-coding.” She raises the possibility that “they are uniquely designed for species- and clade-specific functions” but draws no firm conclusions.

Comments
“65% Unknown (probably mostly junk)”, http://sandwalk.blogspot.ca/20.....enome.html
A beautiful example of an advanced quote-mining technique.* Without checking the source you'd never know that bornagain is partially quoting two successive items from a list and that the "65%" is associated with the previous item, and not with "Unknown". Roy *Which may be due to carelessness rather than unscrupulousnessRoy
November 2, 2015
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bornagain: the coherence of a billion-trillion protein molecules for precisely a life time and not a moment longer is certainly an effect that demands an adequate explanation if ever an effect in science did demand an adequate explanation, i.e. a ’cause’. Well, if we assume that life is due to the coherence of a billion-trillion molecules, then when they cease to cohere, then life would end. We might test whether life is due to such coherence by various experiments to interfere with the coherence; e.g. bullets, poisons, lightning.Zachriel
November 2, 2015
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Yes Box, the coherence of a billion-trillion protein molecules for precisely a life time and not a moment longer is certainly an effect that demands an adequate explanation if ever an effect in science did demand an adequate explanation, i.e. a 'cause'. And as mentioned the other day, the reductive materialistic framework that neo-Darwinists rely on for their explanations is grossly inadequate as to providing any sensible explanation for how it is remotely possible for a billion-trillion protein molecules to cohere as a single unified whole, i.e. a ‘form’, for precisely a lifetime, and not a moment longer. To refresh the point I made,
In fact, until recently it was naively thought that the communication of information in the cell was accomplished primarily when diffusing molecules randomly collided with each other:
“We have always underestimated cells. Undoubtedly we still do today. But at least we are no longer as naive as we were when I was a graduate student in the 1960s. Then, most of us viewed cells as containing a giant set of second-order reactions: molecules A and B were thought to diffuse freely, randomly colliding with each other to produce molecule AB—and likewise for the many other molecules that interact with each other inside a cell. This seemed reasonable because, as we had learned from studying physical chemistry, motions at the scale of molecules are incredibly rapid. … But, as it turns out, we can walk and we can talk because the chemistry that makes life possible is much more elaborate and sophisticated than anything we students had ever considered. Proteins make up most of the dry mass of a cell. But instead of a cell dominated by randomly colliding individual protein molecules, we now know that nearly every major process in a cell is carried out by assemblies of 10 or more protein molecules. And, as it carries out its biological functions, each of these protein assemblies interacts with several other large complexes of proteins. Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines,,, – Bruce Alberts, “The Cell as a Collection of Protein Machines: Preparing the Next Generation of Molecular Biologists,” Cell, 92 (February 6, 1998): 291-294) Editor-in-Chief of Science (2009-2013) served two six-year terms as the president of the National Academy of Sciences
To say that randomly diffusing molecules are grossly inadequate as an explanation for how it is possible for a billion-trillion protein molecules to cohere for a single unified whole, i.e. a ‘form’, for precisely a lifetime, and not a moment longer, is to insult the fact that smoke signals are grossly inadequate as a means of communication for the internet. (i.e. ‘Grossly inadequate’ is to understate the severity of the shortfall in the explanation for how it is possible for a billion-trillion molecules to cohere as a single unified whole.) https://uncommondescent.com/intelligent-design/the-skeptical-zone-asks-what-is-a-code/#comment-585777
The rest of the preceding post goes on to talk about extremely sophisticated biophotonic communication between proteins and DNA in life, and also talks about 'conserved' beyond space and time quantum information being found in molecular biology on a massive scale, (i.e. a 'soul'). But to press the point a little further home, it turns out that the internet itself is akin to communicating via smoke signals when looking at the extremely sophisticated biophotonic communication of life. In other words, the communication of information in life is orders of magnitude more sophisticated than anything man has yet achieved in electronics and the internet! To give some background, 'Photonics', which is in its baby steps of development in computer engineering, offers some very impressive communication advantages over the current method of communicating via electrons.
Photonics Excerpt: Unlike electrons, the driving force behind electronics, photons do not require any copper wires or other barriers to keep them from interacting with one another crossing and mingling photons have no adverse interactions whatsoever, where clashing electronics results in signal confusion and noise.,,, Photonic systems greatly expand the amount of bandwidth available; photonic transmissions are measured in trillion hertz (terahertz), compared with less than 10 billion hertz (gigahertz) used to measure electronics. http://ecommerce.hostip.info/pages/853/Photonics.html
To state the obvious, computer engineers should be absolutely green with envy at how much more advanced biophotonic communication is in biology when compared to the 'primitive' results thus far accomplished in electronics. Of somewhat related note to a billion-trillion protein molecules cohering as a single unified whole for precisely a lifetime and not a moment longer, it is interesting to point out that proteins (and genes), since they are ultimately 'information theoretic' themselves, have rightly been compared to written words. In fact, Dr. Torley made the comparison the other day:
See section on Perry Marshall DNA Language - Human Language Nucleotide - Character Codon - Letter Gene - Word Operon - Sentence Regulon - Paragraph https://uncommondescent.com/intelligent-design/the-skeptical-zone-asks-what-is-a-code/
Obviously, a billion-trillion written words cohering to the single book, i.e. the unified whole, that is a human person, demands an author of far, far greater talent than Shakespeare ever was. My question is, 'just who was, and is, this author of life?' Well, there have been 'rumors' in regards to Whom that author of life must be: Verses, quote and music:
Acts 3:15 You killed the author of life, but God raised him from the dead. We are witnesses of this. John 1:1-4 In the beginning was the Word, and the Word was with God, and the Word was God. He was with God in the beginning. Through him all things were made; without him nothing was made that has been made. In him was life, and that life was the light of all mankind. "There are more things in heaven and earth, Horatio, Than are dreamt of in your philosophy." Shakespeare - Hamlet High School Musical 2 – You are the music in me http://www.youtube.com/watch?v=IAXaQrh7m1o
bornagain
November 2, 2015
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OT — about "form." Bornagain, Just an observation. Human bodily features are not disjoint from each other with respect to the main form — in other words, the 'sub-forms' (often) match in this respect. Albeit on a subtle level, everyone has a body with its own unique "form", which expresses itself coherently in every aspect of it parts. It cannot be measured perhaps, so probably science can safely ignore it, but we can all see it. We see it when things don't match. We also recognize it when it is no longer "real", when it has been tampered with; e.g. plastic surgery. I cannot think of any naturalistic explanation for the coming into existence of a unique coherent human form with every new individual.Box
November 2, 2015
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Dr. Hunter, as to this paper you cited on 'compensatory changes':
Sequence space and the ongoing expansion of the protein universe - June 2010 Excerpt: ~98 per cent of sites cannot accept an amino-acid substitution at any given moment but a vast majority of all sites may eventually be permitted to evolve when other, compensatory, changes occur. http://www.nature.com/nature/journal/v465/n7300/full/nature09105.html#B4
Yet, changes that require two or more coordinated changes to act in combination in order for a change to occur require far too long for evolution to be feasible:
Waiting Longer for Two Mutations - Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that 'for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years' (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.,,, The difficulty with models such as Durrett and Schmidt’s is that their biological relevance is often uncertain, and unknown factors that are quite important to cellular evolution may be unintentionally left out of the model. That is why experimental or observational data on the evolution of microbes such as P. falciparum are invaluable,,, http://www.discovery.org/a/9461 Evolution And Probabilities: A Response to Jason Rosenhouse - August 2011 Excerpt: The equations of population genetics predict that – assuming an effective population size of 100,000 individuals per generation, and a generation turnover time of 5 years – according to Richard Sternberg’s calculations and based on equations of population genetics applied in the Durrett and Schmidt paper, that one may reasonably expect two specific co-ordinated mutations to achieve fixation in the timeframe of around 43.3 million years. When one considers the magnitude of the engineering fete, such a scenario is found to be devoid of credibility. per UD More from Ann Gauger on why humans didn’t happen the way Darwin said - July 2012 Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population. You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes,, in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/ "Enzyme Families -- Shared Evolutionary History or Shared Design?" - Ann Gauger - December 4, 2014 Excerpt: If enzymes can't be recruited to genuinely new functions by unguided means, no matter how similar they are, the evolutionary story is false.,,, Taken together, since we found no enzyme that was within one mutation of cooption, the total number of mutations needed is at least four: one for duplication, one for over-production, and two or more single base changes. The waiting time required to achieve four mutations is 10^15 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. We have now addressed two objections raised by our critics: that we didn't test the right mutation(s), and that we didn't use the right starting point. We tested all possible single base changes in nine different enzymes, Those nine enzymes are the most structurally similar of BioF's entire family We also tested 70 percent of double mutations in the two closest enzymes of those nine. Finally, some have said we should have used the ancestral enzyme as our starting point, because they believe modern enzymes are somehow different from ancient ones. Why do they think that? It's because modern enzymes can't be coopted to anything except trivial changes in function. In other words, they don't evolve! That is precisely the point we are making. http://www.evolutionnews.org/2014/12/a_new_paper_fro091701.html Is Evolution True? Laying Out the Logic - December 4, 2014 In contrast, our argument is as follows: 1. Is evolution true? Test case: do enzymes evolve by a process of natural selection and random mutation? 2. Modern enzymes are the only thing we can test. 3. No one knows if ancient enzymes were different. They are lost in the deep past, so claims with regard to their promiscuity or ability to evolve are hypothetical and unfalsifiable. 4. Modern enzymes can’t evolve new functions, based on our own experiments. 5. We haven’t tested the universe of modern enzymes, so our result is qualified, but the nine most similar enzymes did not change function. 6. Our estimate for the likely waiting time for an enzyme to evolve a new function is at least 10^15 years. 7. Therefore evolution of enzymes is likely to be impossible. 8. Given the sophistication of enzymes and the way they work together, intelligent design is the best explanation for the origin and current diversity of modern enzymes. http://www.biologicinstitute.org/post/104413161394/is-evolution-true-laying-out-the-logic "Shared Evolutionary History or Shared Design?" - Ann Gauger - January 1, 2015 Excerpt: The waiting time required to achieve four mutations is 10^15 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. http://www.evolutionnews.org/2015/01/happy_new_year092291.html Thou Shalt Not Put Evolutionary Theory to a Test - Douglas Axe - July 18, 2012 Excerpt: "For example, McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time (i.e. the mutations cannot be 'neutral'). Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (greater than 100 million years). My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they're in the position of insisting that something is a scientific fact without having the faintest idea how it even could be." Doug Axe PhD. http://www.evolutionnews.org/2012/07/thou_shalt_not062351.html "Lynch and Abegg assumed [in their paper] that organisms will acquire a given complex adaptation by traversing a direct path to the new anatomical structure. Each mutation would build on the previous one in the most efficient manner possible – with no setbacks, false starts, aimless wandering, or genetic degradation – until the desired structure or system (or gene) is constructed. Thus, they formulated an undirected model of evolutionary change, and one that assumes, moreover, that there is no mechanism available (such as natural selection) that can lock in potentially favorable mutational changes on the way to some complex advantageous structure…. Yet nothing in Lynch’s neutral model ensures that potentially advantageous mutations will remain in place while other mutations accrue. As Axe explains [in his reply to Lynch], “Productive changes cannot be ‘banked,’ whereas Equation 2 [one of Lynch’s equations] presupposes that they can.” Instead, Axe shows, mathematically, that degradation (the fixation of mutational changes that make the complex adaptation less likely to arise) will occur much more rapidly than constructive mutations, causing the expected waiting time to increase exponentially." Stephen Meyer - Darwin”s Doubt - Harper One, 2013, p. 328,
Of related interest, here are a few more empirical observations from Behe
Peer-reviewed paper: Michael Behe’s “First Rule of Adaptive Evolution” - Oct. 30, 2015 Excerpt: “The First Rule of Adaptive Evolution”: “Break or blunt any functional coded element whose loss would yield a net fitness gain.” In essence, what Behe means is that mutations that cause loss-of-FCT are going to be far more likely and thus far more common than those which gain a functional coding element. http://winteryknight.com/2015/10/30/peer-reviewed-paper-michael-behes-first-rule-of-adaptive-evolution/ From Thornton's Lab, More Strong Experimental Support for a Limit to Darwinian Evolution - Michael Behe - June 23, 2014 Excerpt: In prior comments on Thornton's work I proposed something I dubbed a "Time-Symmetric Dollo's Law" (TSDL).3, 8 Briefly that means, because natural selection hones a protein to its present job (not to some putative future or past function), it will be very difficult to change a protein's current function to another one by random mutation plus natural selection. But there was an unexamined factor that might have complicated Thornton's work and called the TSDL into question. What if there were a great many potential neutral mutations that could have led to the second protein? The modern protein that occurs in land vertebrates has very particular neutral changes that allowed it to acquire its present function, but perhaps that was an historical accident. Perhaps any of a large number of evolutionary alterations could have done the same job, and the particular changes that occurred historically weren't all that special. That's the question Thornton's group examined in their current paper. Using clever experimental techniques they tested thousands of possible alternative mutations. The bottom line is that none of them could take the place of the actual, historical, neutral mutations. The paper's conclusion is that, of the very large number of paths that random evolution could have taken, at best only extremely rare ones could lead to the functional modern protein. http://www.evolutionnews.org/2014/06/more_strong_exp087061.html
bornagain
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Kairosfocus (482): The rugged and flat nature of the protein evolution fitness landscape comes from both theoretical and experimental considerations, and from native sequences as well as random sequences. Studies attempting to blindly evolve protein sequences from random sequences find that an astronomical number of starting points are needed to get close enough in order for selection to do the job: http://www.sciencedirect.com/science/article/pii/0022519377900443 http://www.ncbi.nlm.nih.gov/pubmed/2199970 http://www.ncbi.nlm.nih.gov/pubmed/15321723 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000096 Yet even absurdly optimistic studies show that evolution has nowhere near such astronomical resources: http://rsif.royalsocietypublishing.org/content/5/25/953.long And while a given protein may come in very different sequences, only a few percent of changes to that sequence can be sustained. See, for example: http://www.ncbi.nlm.nih.gov/pubmed/19765975 http://www.nature.com/nature/journal/v465/n7300/full/nature09105.html#B4 For a summary see this post of mine: http://darwins-god.blogspot.com/2015/09/yockey-and-calculator-versus.htmlCornelius Hunter
November 1, 2015
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Serendipity Theory. I like it.Mung
November 1, 2015
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@Cornelius: Still waiting for you to address post #458.ThickPython
November 1, 2015
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Python, I guess you missed the whole argument after that point? which was, "even if I did accept that 98% figure it still does not go one inch towards telling us how it is remotely possible to transform a chimp-like creature into a human." How did I know that you would refuse to address the elephant in the living room problem of 'form' for materialistic explanations and reiterate the 98% figure? even after I conceded the figure for the sake of argument so as to emphasize and focus on my main point? i.e. Materialistic explanations are a non-starter in any 'theory of transformation'. But I guess being honest to that fact is just something that you refuse to even consider since it clearly leads to a Theistic answer huh?bornagain
November 1, 2015
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@BornAgain, #521:
... due too biased methodology in genetic tree construction, I certainly have reasons to doubt the integrity of the 98% figure
The 98% figure has nothing to do with phylogenetic tree construction. You need three species at a minimum to do any sort of phylogenetic work, while the chimpanzee to human figure of 98% is just a comparison of two species. Just line them up as best you can, and count the bases that are the same. Can you tell us all why you doubt the 98% figure?ThickPython
November 1, 2015
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VJ (516): ================== Effectively, you’ve conceded that you have no good grounds for believing that the de novo genes recently found in human beings, or the proteins that they code for, were in fact designed. ================== In my Comment #476 I explained that one of your questions for me was a non sequitur. Now here we have it again. I never said they were “designed.” Beginning with the OP, you seem to be intent on putting words in my mouth and then making accusations based on these strawmen. ================== However, it doesn’t follow from this that all proteins were designed. ================== Another non sequitur. ================== You then criticize the Nature article’s attempt to explain the origin of de novo proteins on the grounds that it would require “an army of proteins in order to achieve protein evolution.” That’s a fair point, but all it shows is that some proteins (in particular, the first proteins) must have been designed in the first place, in order for new ones to evolve. However, it doesn’t follow from this that all proteins were designed. ================== No, I think you have missed the serendipity required. The problem here is not merely that protein evolution is unlikely due to, for example, the rugged and flat fitness landscapes. In addition to this, the various protein evolution mechanisms that evolutionists envision (horizontal gene transfer followed by mutations, duplication followed by mutations, de novo gene birth such as described by the Vidal paper, etc.) all require elaborate, intricate, complex mechanisms to have evolved which, in the end, could create new proteins. Creating those new proteins would turn out to be really great for the evolutionary progress, fitness of the organisms, etc. But how would evolution and natural selection know this in advance? Selection only knows about the immediate, current, mutation. It doesn’t know that this, plus a million more mutations, will give me a whole new way of making proteins. So evolutionists must say there were some other benefits to creating each little piece of molecular machinery, and then just luckily, serendipitously, it all came together in the end to yield HGT, duplication, de novo, etc., mechanisms for creating proteins. That is an enormous quantity of serendipity and theory complexity, far beyond what can fairly be ascribed to evolutionary theory. So, no, the problem is not merely the evolution of the first proteins. ================== You also write that “protein fitness landscapes are flat and rugged, not smooth and sloped.” Again: this may be true of most proteins, but we don’t know if it’s true for those proteins which are unique to humans. ================== This is, again, looking at nature from an evolutionary perspective. It is not exactly a mystery why protein evolution landscapes are rugged and from a *scientific* perspective there is no reason to think that a fitness landscape would suddenly be smooth and sloped just for those proteins that are unique to humans. This is nothing more than special pleading, with no basis in science. Furthermore, as is typical of evolutionary explanations, it is a one-off explanation. The Vidal paper deals with yeast, for example.Cornelius Hunter
November 1, 2015
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501 Larry MoranOctober 31, 2015 at 7:42 pm Nick Matzke said, "It’s debatable whether it’s costly, at least for large multicellular organisms." No, it’s not really debatable. What you meant to say is that it may not be VERY costly compared to other expenses. That’s not the same thing at all. Arguably, in everyday usage, "costly" means something like "significant cost compared to everything else costing something". But as long as we agree that, in some organisms at least, DNA replication is a very small cost compared to numerous other costs, that's enough for the argument to proceed. (Besides, the argument you presented doesn’t apply to large multicellular plants.) I would love to get some cellular metabolism person to do the calculation and calculate the ballpark cost of DNA replication per-base in terms of energy (ATP), N, etc. -- and then compare this to ballpark figures for protein synthesis, metabolism in various cells, etc. For plants, I bet the big costs are things like cellulose production. And I bet they are way bigger than the cost of DNA replication. I suspect that straight-up weighing the mass of cellulose per cell and the mass of DNA per cell would give a ballpark estimate of the energetic costs of each. The question before us is why junk DNA isn’t eliminated if it’s really junk and there’s any cost all associated with retaining it in the genome. Natural selection should have eliminated anything that has even the slightest cost, right? I know the answer, but let's see if any of the creationists here can even state the standard population genetics answer to this question.NickMatzke_UD
November 1, 2015
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Dr. Moran, despite your protests to the contrary, your internet persona betrays you mightily. But what would I know? I'm only a IDiot. Who am I to question the superior intellect of a person who does not even really exist? at 37:51 minute mark of following video, according to the law of identity, Richard Dawkins does not exist as a person: (the unity of Aristotelian Form is also discussed) i.e. ironically, in atheists denying that God really exists, they end up denying that they themselves really exist as real persons.
Atheistic Materialism – Does Richard Dawkins Exist? – video Quote: "It turns out that if every part of you, down to sub-atomic parts, are still what they were when they weren't in you, in other words every ion,,, every single atom that was in the universe,, that has now become part of your living body, is still what is was originally. It hasn't undergone what metaphysicians call a 'substantial change'. So you aren't Richard Dawkins. You are just carbon and neon and sulfur and oxygen and all these individual atoms still. You can spout a philosophy that says scientific materialism, but there aren't any scientific materialists to pronounce it.,,, That's why I think they find it kind of embarrassing to talk that way. Nobody wants to stand up there and say, "You know, I'm not really here". https://www.youtube.com/watch?v=rVCnzq2yTCg&t=37m51s
At the 23:33 minute mark of the following video, Richard Dawkins agrees with materialistic philosophers who say that:
"consciousness is an illusion"
A few minutes later Rowan Williams asks Dawkins
”If consciousness is an illusion…what isn’t?”. https://www.youtube.com/watch?v=HWN4cfh1Fac&t=22m57s
A few more notes (of many)
The Atheist’s Guide to Intellectual Suicide – James N. Anderson PhD. - video https://vimeo.com/75897668 "Hawking’s entire argument is built upon theism. He is, as Cornelius Van Til put it, like the child who must climb up onto his father’s lap into order to slap his face. Take that part about the “human mind” for example. Under atheism there is no such thing as a mind. There is no such thing as understanding and no such thing as truth. All Hawking is left with is a box, called a skull, which contains a bunch of molecules. Hawking needs God In order to deny Him." - Cornelius Hunter Photo – an atheist contemplating his mind http://3.bp.blogspot.com/-H-kjiGN_9Fw/URkPboX5l2I/AAAAAAAAATw/yN18NZgMJ-4/s1600/rob4.jpg
bornagain
November 1, 2015
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Yet it is exactly this type of ‘traveling salesman problem’, i.e. NP complete problem, that quantum computers excel at:
Speed Test of Quantum Versus Conventional Computing: Quantum Computer Wins – May 8, 2013 Excerpt: quantum computing is, “in some cases, really, really fast.” McGeoch says the calculations the D-Wave excels at involve a specific combinatorial optimization problem, comparable in difficulty to the more famous “traveling salesperson” problem that’s been a foundation of theoretical computing for decades.,,, “This type of computer is not intended for surfing the internet, but it does solve this narrow but important type of problem really, really fast,” McGeoch says. “There are degrees of what it can do. If you want it to solve the exact problem it’s built to solve, at the problem sizes I tested, it’s thousands of times faster than anything I’m aware of. If you want it to solve more general problems of that size, I would say it competes — it does as well as some of the best things I’ve looked at. At this point it’s merely above average but shows a promising scaling trajectory.” per Science Daily Scientists achieve critical steps to building first practical quantum computer – April 30, 2015 Excerpt: If a quantum computer could be built with just 50 quantum bits (qubits), no combination of today’s TOP500 supercomputers could successfully outperform it (for certain tasks). http://phys.org/news/2015-04-scientists-critical-quantum.html
That proteins have the inherent ability to perform quantum computation, and thus provide an adequate solution to the protein folding enigma, is established by the fact that proteins are now found to have quantum information embedded within them:
Classical and Quantum Information Channels in Protein Chain – Dj. Koruga, A. Tomi?, Z. Ratkaj, L. Matija – 2006 Abstract: Investigation of the properties of peptide plane in protein chain from both classical and quantum approach is presented. We calculated interatomic force constants for peptide plane and hydrogen bonds between peptide planes in protein chain. On the basis of force constants, displacements of each atom in peptide plane, and time of action we found that the value of the peptide plane action is close to the Planck constant. This indicates that peptide plane from the energy viewpoint possesses synergetic classical/quantum properties. Consideration of peptide planes in protein chain from information viewpoint also shows that protein chain possesses classical and quantum properties. So, it appears that protein chain behaves as a triple dual system: (1) structural – amino acids and peptide planes, (2) energy – classical and quantum state, and (3) information – classical and quantum coding. Based on experimental facts of protein chain, we proposed from the structure-energy-information viewpoint its synergetic code system. http://www.scientific.net/MSF.518.491
And 'quantum information' is the ‘physical resource’ by which quantum computation is accomplished:
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/
And in fact, protein folding is now found to belong to the quantum physics, not classical physics:
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.,,, Today, Luo and Lo say these curves can be easily explained if the process of folding is a quantum affair. By conventional thinking, a chain of amino acids can only change from one shape to another by mechanically passing though various shapes in between. But Luo and Lo say that if this process were a quantum one, the shape could change by quantum transition, meaning that the protein could ‘jump’ from one shape to another without necessarily forming the shapes in between.,,, 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/
Moreover, in a finding that would have pleased Erwin Schrodinger very much, quantum coherence was just empirically verified to be within proteins a few weeks ago:
Quantum coherent-like state observed in a biological protein for the first time - October 13, 2015 Excerpt: If you take certain atoms and make them almost as cold as they possibly can be, the atoms will fuse into a collective low-energy quantum state called a Bose-Einstein condensate. In 1968 physicist Herbert Fröhlich predicted that a similar process at a much higher temperature could concentrate all of the vibrational energy in a biological protein into its lowest-frequency vibrational mode. Now scientists in Sweden and Germany have the first experimental evidence of such so-called Fröhlich condensation (in proteins).,,, The real-world support for Fröhlich's theory (for proteins) took so long to obtain because of the technical challenges of the experiment, Katona said. http://phys.org/news/2015-10-quantum-coherent-like-state-biological-protein.html
To be clear, quantum coherence, like entanglement, is a beyond space and time, i.e. 'non-local', effect:
Coherence and nonlocality Usually quantum nonlocality is discussed in terms of correlated multiparticle systems such as those discussed by John Bell in his famous 1964 theorem and then later clarified by GHZ, David Mermin and others. But more striking and significant is the qualitative nonlocal phenomena associated with coherent states,,,, In fact, theoretically these two kinds of nonlocality have precisely the same basis: the unmeasured singlet state uncovered by EPR is a coherent 'pure state' despite its spacial extension, and when the parts are realized in a measurement (a la Bell) this coherence is harvested or cashed in. Whereas the "EPR" connections are ephemeral and fragile, some forms of nonlocal coherence are robust. http://www.nonlocal.com/hbar/nonlocalcoherence.html
Thus, since the shape of the protein itself cannot be explained without appeal to a beyond space and time cause, how in blue blazes is it possible for reductive materialistic explanations to be the explanation for the shape of an entire human? Much less explain the transformation of some chimp-like creature into a human? Materialistic explanations are simply bankrupt before they even get out of the starting gate in trying to explain such a gargantuan task! Verse and Music:
John 1:1-4 In the beginning was the Word, and the Word was with God, and the Word was God. He was with God in the beginning. Through him all things were made; without him nothing was made that has been made. In him was life, and that life was the light of all mankind. High School Musical 2 - You are the music in me http://www.youtube.com/watch?v=IAXaQrh7m1o
bornagain
November 1, 2015
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Although, as mentioned previously, due too biased methodology in genetic tree construction, I certainly have reasons to doubt the integrity of the 98% figure, even if I did accept that 98% figure it still does not go one inch towards telling us how it is remotely possible to transform a chimp-like creature into a human. As Dr. Nelson recently put the nature of the problem,
What Evolution Is, and What It's Not - Paul Nelson - October 30, 2015 Excerpt: "Evolution, in the sense of common descent, is not a theory of similarity. Linnaeus, Cuvier, and Agassiz knew all about similarity, yet they denied common descent. Evolution is a theory of transformation.",,, and "If the overall biology of the animals tells you that they are very different, and the genetics tells you that they are nearly identical, it follows that the genetic comparison is telling you something relatively trivial about the overall biology." Jonathan Marks http://www.evolutionnews.org/2015/10/what_evolution100501.html
As mentioned previously in this very thread, there are some insurmountable 'poly-constrained' difficulties (Sanford) for the gradualistic 'theory of transformation' that should rightly raise some puzzled eyebrows. Here is my post on some of those insurmountable difficulties:
Common Descent? - Some Insurmountable Problems for the theory of gradualism and/or transformation https://docs.google.com/document/d/1BBU4GVEPIxDDSre6YLqU5zbaXVdSk4RRMD8F7GU3DPM/edit
Moreover, as outlined in your other thread yesterday Dr. Torley, we also have very good reasons, (evidential and logical), to posit the necessity of, of all things, a 'soul' so as to be able to explain how in blue blazes it is even remotely possible for the billion-trillion protein molecules of the human body to cohere as a single unified whole "for precisely a lifetime, and not a moment longer?" (Talbott):
“You don’t have a soul. You are a soul. You have a body.” George MacDonald – Annals of a Quiet Neighborhood – 1892 https://uncommondescent.com/intelligent-design/the-skeptical-zone-asks-what-is-a-code/#comment-585777
But apparently the severity of the problem has not gotten through yet Dr. Torley since you keep bringing up the 98% figure as if that genetic similarity even begins to answer the question of how is it remotely possible to transform a one creature into another creature. It doesn't even begin! So let's go a little deeper. Reductive materialism cannot even explain how a protein achieves its unique shape. Thus how much less can reductive materialism explain how it is possible to transform one creature into another creature? First off in highlighting this problem, many proteins have no intrinsic shape, (intrinsically disordered proteins), taking on different roles in different molecular 'contexts':
“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, (intrinsically disordered proteins), 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
"Context", to put it mildly, is not a minor problem for reductive materialistic explanations. Moreover, as if that was not bad enough for materialists, protein folding itself cannot be reduced to reductive materialistic explanations. Specifically, it is now known that proteins do not find their final folded form by a random search as would be expected in a neo-Darwinian view of things:
The Humpty-Dumpty Effect: A Revolutionary Paper with Far-Reaching Implications – Paul Nelson – October 23, 2012 Excerpt: Anyone who has studied the protein folding problem will have met the famous Levinthal paradox, formulated in 1969 by the molecular biologist Cyrus Levinthal. 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. Therefore, concluded Levinthal, given that proteins obviously do fold, they are doing so, not by random search, but by following favored pathways. The challenge of the protein folding problem is to learn what those pathways are. http://www.evolutionnews.org/2012/10/a_revolutionary065521.html Confronting Science’s Logical Limits – John L. Casti – 1996 Excerpt: It has been estimated that a supercomputer applying plausible rules for protein folding would need 10^127 years to find the final folded form for even a very short sequence consisting of just 100 amino acids. (The universe is 13.7 x 10^9 years old). In fact, in 1993 Aviezri S. Fraenkel of the University of Pennsylvania showed that the mathematical formulation of the protein-folding problem is computationally “hard” in the same way that the traveling-salesman problem is hard. http://www.cs.virginia.edu/~robins/Confronting_Sciences_Logical_Limits.pdf
The reason why finding the final form of a folded protein is so hard for supercomputers is that it is like the ‘traveling salesman’ puzzle, which are ‘Just about the meanest problems you can set a computer (on) ‘.
DNA computer helps traveling salesman – Philip Ball – 2000 Excerpt: Just about the meanest problems you can set a computer belong to the class called ‘NP-complete’. The number of possible answers to these conundrums, and so the time required to find the correct solution, increases exponentially as the problem is scaled up in size. A famous example is the ‘travelling salesman’ puzzle, which involves finding the shortest route connecting all of a certain number of cities.,,, Solving the traveling-salesman problem is a little like finding the most stable folded shape of a protein’s chain-like molecular structure — in which the number of ‘cities’ can run to hundreds or even thousands. http://www.nature.com/news/2000/000113/full/news000113-10.html
And protein folding is indeed found to be a ‘NP-complete’ problem
Combinatorial Algorithms for Protein Folding in Lattice Models: A Survey of Mathematical Results – 2009 Excerpt: Protein Folding: Computational Complexity 4.1 NP-completeness: from 10^300 to 2 Amino Acid Types 4.2 NP-completeness: Protein Folding in Ad-Hoc Models 4.3 NP-completeness: Protein Folding in the HP-Model http://www.cs.brown.edu/~sorin/pdfs/pfoldingsurvey.pdf
bornagain
November 1, 2015
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bornagain says,
UCLA Scientists Find 3000 New Genes in “Junk DNA” of Immune Stem Cells – October 28, 2015 Excerpt: Not Junk After All
I blogged about this paper at ... 3,000 new genes discovered in the human genome - dark matter revealed More stupid hype about lncRNAs You're more than welcome to participate in the discussion on my blog as long as you stick to the science. You can start by explaining why those 3,000 sequences are "genes." Then you can address the point I made about the amount of the genome that's being discussed. Even if all 3,000 sequences were functional genes (they are not), it would only amount to 0.1% of the genome. Do you think that's significant?Larry Moran
November 1, 2015
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bornagain asks,
As well Dr. Moran, if you have not noticed, you are infamous among people on the internet as having an irrational hatred towards people who believe life is designed, (i.e. whom you constantly insult with the term “IDiots”), and especially towards God in particular. Why this irrational, ‘illogical’, hatred Dr. Moran?
I'm on quite friendly terms with Michael Behe having met him several times. I do not hate him and I usually avoid calling him an IDiot although I may have gotten exasperated on one or two occasions. I respect the way Micheal Behe argues his case and I respect Michael Denton as well. I've met and corresponded with Bill Dembski and I don't hate him at all. I think he's a very sincere fellow. Lot's of people may hate theists but I'm not one of them even though I think they are misguided. You probably haven't noticed but I usually restrict the term IDiots to Intelligent Design Creationists who act like idiots. You, for example. Is it irrational to dislike some of the people who comment about me on this blog? I don't think so. For example, it's hard to think of you as a friend when you say (#499)
I’m sure you can, just mouth the syllables very slowly Dr. Moran. ves·tig·i·al or·gans There you go, that’s a good boy. You are making good progress!
I'm also struggling (unsuccessfully) to think good thoughts about Andre when he says (#67, #119),
I am now convinced that Prof Larry Moran is an idiot. The issue is not evolution per say Prof Moran the issue is unguided vs. guided. How does one model unguided evolution? Please tell us Prof Moran? How does unguided processes create guided processes to prevent unguided processes from happening in the first place? The mind boggles that a supposedly intelligent being can be so utterly dumb.
I don't mind the insults and the cut-and-thrust of internet debates. It's part of the fun. I'm an alumnus of talk.origins, which invented internet insults. What I detest is hypocrisy, like when Intelligent Design Creationists whine about being called IDiots then turn around and hurl abuse at evolutionary biologists and other scientists who disagree with them.Larry Moran
November 1, 2015
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Arthur Hunt:
Cells have a variety of mechanisms for getting rid of damaged or other inappropriate RNAs and proteins.
And just how does unguided evolution, ie drift and natural selection, account for that?Virgil Cain
November 1, 2015
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Larry Moran: Junk DNA is not compatible with classic Darwinian evolution.
Whatever Larry. A more fundamental point would be that naturalism cannot ground junk-DNA, because naturalism cannot distinguish between function and non-function. IOW naturalism cannot ground "function". // If there is no external function imposed on organisms then in order for function to exist it must be internally grounded in a hierarchical whole-parts-relationship; in which the parts are submissive (functional) to the whole. The realness of function depends on the realness of this hierarchical relationship. The hierarchical relationship in biology is only real if there is a real whole with real causal power; distinct from the parts. In other words a theory cannot speak coherently of function if it cannot ground the independent ontological reality of the whole. // The argument from internal biological function // 1. Internal function can only exist in the context of a hierarchical relationship between the whole and the parts. 2. Naturalism cannot ground the existence of such a whole. 3. Internal function in biology is real. 4. Naturalism cannot ground internal function. (1,2 & 3) Conclusion: naturalism is false. //Box
November 1, 2015
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Dr. Hunter, Thank you for your posts. In your response (#476), you criticized my assertion that chimpanzee DNA contains (non-coding) sequences which are 98% similar to protein-coding genes that are unique to humans, and you wrote:
The chimp and ape non-coding DNA is not 98% similar to the human protein-coding gene, and there was no “98%-similar homolog” to a protein-coding gene.
But when Nick Matzke (who has a Ph.D. in evolutionary biology from Berkeley) challenged you on that point (see post #480 above), saying,
It sounds like it is, or something close to that...
...and then went on to offer no less than three possible interpretations of the findings about protein-coding genes that are unique to humans from an evolutionary standpoint, suggesting that the proteins coded for may not be as specific as normal proteins, you then backed down from your position and wrote back to him:
I never said such interpretations are implausible. In fact my original point was *if* these proteins are like most proteins, then blah, blah, blah.
Effectively, you've conceded that you have no good grounds for believing that the de novo genes recently found in human beings, or the proteins that they code for, were in fact designed. You then criticize the Nature article's attempt to explain the origin of de novo proteins on the grounds that it would require "an army of proteins in order to achieve protein evolution." That's a fair point, but all it shows is that some proteins (in particular, the first proteins) must have been designed in the first place, in order for new ones to evolve. However, it doesn't follow from this that all proteins were designed. You also write that "protein fitness landscapes are flat and rugged, not smooth and sloped." Again: this may be true of most proteins, but we don't know if it's true for those proteins which are unique to humans.vjtorley
November 1, 2015
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Mung, I think I understand you now. You're saying that there's a non-zero probability that someone writing a program will make a mistake, resulting in a bug. Having been a computer programmer for ten years (1989-1999), I would have to agree. And of course, if the bug is a mathematical one, then it will generate mathematically absurd results - like the ones obtained by Dr. Tomkins (which he should have noticed).vjtorley
November 1, 2015
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VJ Torley:
It’s mathematically impossible for two times 28 to equal 124.
You misunderstand my argument. My argument was that the probability of the results obtained by Tomkins were obviously not "exactly zero", because he did in fact get those results. Due to a bug in the software. See this exchange: bornagain: So ‘mathematically impossible’ has nothing whatsoever to do with probability? ThickPython: In the context of my paper, that’s correct. The probability of getting these results – where 200bp slices have 62% identity and 100 bp slices have 24% identity – is exactly zero. It’s not one chance in 2 ^ 500. It’s zero. It’s mathematically impossible. Perhaps ThickPython was just having a bad day. Edited to add:
The probability of getting 62% identity (i.e. 124 identical nucleotides) for a 200 bp slice which is composed of two 100 bp slices that each have 28 identical nucleotides on average is indeed “exactly zero.” It can’t happen. - VJT
And yet it did happen, or we would not be here talking about it.Mung
November 1, 2015
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Dr. Moran, your reasoning is DEFINITELY NOT based on very solid scientific evidence and logic. I could list the specific details for why each of your points fail, but alas, you would just call me an IDiot and not listen any way, so what is the point? But one quick observation, before you can claim that you are using reasoning and logic to support your atheistic worldview, would it not be VERY helpful if you could first ground reasoning and logic in your atheistic worldview? Does this gaping hole in your 'reasoning' even ring a bell anywhere in your head? Or is this huge, gaping, hole in your worldview just another inconvenient truth that you ignore like so many of the other glaring problems in your arguments?
Sam Harris's Free Will: The Medial Pre-Frontal Cortex Did It - Martin Cothran - November 9, 2012 Excerpt: There is something ironic about the position of thinkers like Harris on issues like this: they claim that their position is the result of the irresistible necessity of logic (in fact, they pride themselves on their logic). Their belief is the consequent, in a ground/consequent relation between their evidence and their conclusion. But their very stated position is that any mental state -- including their position on this issue -- is the effect of a physical, not logical cause. By their own logic, it isn't logic that demands their assent to the claim that free will is an illusion, but the prior chemical state of their brains. The only condition under which we could possibly find their argument convincing is if they are not true. The claim that free will is an illusion requires the possibility that minds have the freedom to assent to a logical argument, a freedom denied by the claim itself. It is an assent that must, in order to remain logical and not physiological, presume a perspective outside the physical order. http://www.evolutionnews.org/2012/11/sam_harriss_fre066221.html Atheists embarrassed: study proves atheism uses less brain function – Oct 26, 2015 by Dr. Joel McDurmon Excerpt: This has to be embarrassing . . . if you’re an atheist. A new study performed at the University of York used targeted magnetism to shut down part of the brain. The result: belief in God disappeared among more than 30 percent of participants. That in itself may not seem so embarrassing, but consider that the specific part of the brain they frazzled was the posterior medial frontal cortex—the part associated with detecting and solving problems, i.e., reasoning and logic. In other words, when you shut down the part of the brain most associated with logic and reasoning, greater levels of atheism result. You’ve heard the phrase, “I don’t have enough faith to be an atheist”? Apparently we can now also say, “I have too many brains to be an atheist.” For a group that makes so much noise vaunting its superior prowess with logic and reasoning, this study has got to be quite a deflator. For a group that claims to be rooted primarily in logic and reason, and to exist for little reason other than that they have used logic and reason to free themselves from belief in God and, as they allege, superstition and fairy tales, this study is the equivalent of a public depanting­—i.e., the would-be emperor’s got no clothes. http://americanvision.org/12630/atheists-embarrassed-study-proves-atheism-uses-less-brain-function/ Romans 1:28 Furthermore, just as they did not think it worthwhile to retain the knowledge of God, so God gave them over to a depraved mind, so that they do what ought not to be done.
As well Dr. Moran, if you have not noticed, you are infamous among people on the internet as having an irrational hatred towards people who believe life is designed, (i.e. whom you constantly insult with the term "IDiots"), and especially towards God in particular. Why this irrational, 'illogical', hatred Dr. Moran?
When Atheists Are Angry at God – 2011 Excerpt: I’ve never been angry at unicorns. It’s unlikely you’ve ever been angry at unicorns either.,, The one social group that takes exception to this rule is atheists. They claim to believe that God does not exist and yet, according to empirical studies, tend to be the people most angry at him. http://www.firstthings.com/onthesquare/2011/01/when-atheists-are-angry-at-god Study explores whether atheism is rooted in reason or emotion – Jan. 2015 Excerpt: “A new set of studies in the Journal of Personality and Social Psychology finds that atheists and agnostics report anger toward God either in the past or anger focused on a hypothetical image of what they imagine God must be like. Julie Exline, a psychologist at Case Western Reserve University and the lead author of this recent study, has examined other data on this subject with identical results. Exline explains that her interest was first piqued when an early study of anger toward God revealed a counterintuitive finding: Those who reported no belief in God reported more grudges toward him than believers.” https://uncommondescent.com/just-for-fun/fun-study-explores-whether-atheism-is-rooted-in-reason-or-emotion/
bornagain
November 1, 2015
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Adding another set of evidence to Larry's list: Cells have a variety of mechanisms for getting rid of damaged or other inappropriate RNAs and proteins. It turns out that, if one cripples the mechanisms that act on RNAs, then the products of transcription of junk DNA increase in abundance. These sorts of studies strongly indicate that junk DNA has no role or function. To mix some metaphors - junk = garbage. If one closes the garbage disposal, garbage accumulates. This is what is seen in living cells, and is one reason why it is correct to call large swaths of the typical eukaryotic genome junk.Arthur Hunt
November 1, 2015
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Umm classic Darwinian evolution includes drift as Darwin talked about drift in "On the Origins of Species...". So it appears that Larry is ignorant of what Darwin wrote. As for a strawman version of evolutionary theory-> seeing there isn't any such theory they would all be strawman arguments.Virgil Cain
November 1, 2015
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In my post on What's in Your Genome I attempt to cover everything that's known about functional regions in the human genome. At the end of the post I mention that there's still about one quarter of the genome—mostly intergenic sequences—that don't fit into any category of known junk DNA or functional regions. I said, "Unknown (probably mostly junk) = 26.3%" bornagain (#499) says,
“65% Unknown (probably mostly junk)”, http://sandwalk.blogspot.ca/20.....enome.html Glad to see you making such a concerted attempt to understand the genome before you state its ‘(probably mostly junk)’ Dr. Moran. Perhaps you can excuse the rest of us who don’t buy your argument from ignorance? Or are you 100% positive that your ignorance of functionality constitutes irrefutable proof for Darwinian evolution?
There's a reason why I think that the last 26% is mostly junk and it's based on very solid scientific evidence and logic—things like the genetic load argument, sequence conservation, and deductions from comparative genomics (C-Value Paradox). These are all described in many scientific publications as well as numerous posts on my blog. I find that many of those who argue against junk DNA are ignorant of the basic facts outlined in my blog post and ignorant of the logical explanations accounting for the last 26% of our genome. Thus, it seems to me that it's those people who are basing their arguments on ignorance, not me. I know I've said this many times but it's worth repeating one more time in an attempt to educate IDiots. Junk DNA is not compatible with classic Darwinian evolution. Scientists who continue to adhere to strict "Darwinism" are generally opposed to the idea that most of our genome is junk. No knowledgeable scientist would ever use an argument for junk DNA as "irrefutable proof for Darwinian evolution" (i.e. evolution by natural selection). That doesn't stop IDiots from constantly repeating this false strawman version of evolutionary theory. (See Denyse O'Leary's post on Suzan Mazur’s Paradigm Shifters is now available from Amazon for the standard ID version of "neo-Darwinism" (="Darwinism").)Larry Moran
November 1, 2015
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Cartoon - "Just because you don't understand us, you can't call us junk" https://aholdencirm.files.wordpress.com/2015/10/junk-dna-series2.gif?w=600&h=600 UCLA Scientists Find 3000 New Genes in “Junk DNA” of Immune Stem Cells - October 28, 2015 Excerpt: Not Junk After All Now back to “Junk DNA”… scientists thought that because this mass of DNA sequences was never turned into protein, it served no purpose. It turns out that they couldn’t be farther from the facts.,,, Using sequencing technology and bioinformatics, they mapped the RNA landscape (known as the transcriptome) of rare stem cells isolated from human bone marrow (hematopoietic stem cells) and the thymus (lymphoid progenitor cells). They identified over 9000 genes that produced lncRNAs that were important for moderating various stages of immune cell development. Of this number, over 3000 were genes whose lncRNAs hadn’t been found before.,,, If the pace keeps up, the term “Junk DNA” will need to be retired to the junk yard. http://blog.cirm.ca.gov/2015/10/28/ucla-scientists-find-3000-new-genes-in-junk-dna-of-immune-stem-cells/
bornagain
November 1, 2015
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Mung, I hate to break it to you, but ThickPython is absolutely correct, regarding the mathematical error he identified in Dr. Tomkins' work. Let's have a look at what TP wrote:
Put more simply, a 200 base slice that has – on average – 124 identical nucleotides cannot be split into two 100 base slices that each have – on average – only 28 identical nucleotides. That’s mathematically impossible.
Two times 28 equals 56. It's mathematically impossible for two times 28 to equal 124. The "on average" part doesn't make any difference. If there are 27 identical nucleotides in slice A and 29 identical nucleotides in slice B, then once again we get 27 + 29 + 56. The average for the two slices is 28 identical nucleotides. The probability of getting 62% identity (i.e. 124 identical nucleotides) for a 200 bp slice which is composed of two 100 bp slices that each have 28 identical nucleotides on average is indeed "exactly zero." It can't happen.vjtorley
November 1, 2015
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@Mung: From post #26:
... read the section that discusses the mathematical impossibility of Tomkins getting the results he did. This should have been a blazing neon sign that there was something wrong with the software.
From post #405:
... he is the only one incompetent enough to publish results that are – on their face – mathematically impossible.
Now normally I give people the benefit of the doubt and assume they are just a bit slow on the uptake rather than a troll, but in this case, I REALLY hope you are a troll ... because I would worry for the fate of the human race if you weren't.ThickPython
November 1, 2015
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Larry Moran wrote:
I claim that the average ID proponent cannot describe the standard explanations for junk DNA, and the evidence supporting junk DNA, in spite of the fact that they are more than willing to declare that “Darwinists” are wrong about junk DNA. Here’s good opportunity for Andre to prove that I’m wrong. Write a short, one paragraph, summary of what knowledgeable evolutionary biologists say about the idea that cells can “lug around” lots of junk DNA. I’d really appreciate it if Andre or some of the rest of you could honestly try to prove that I am wrong. Not holding my breath …
So I Googled, "why do some organisms have more junk DNA than others" and came up with a Website which answered the question, "Why do Eukaroytes have so much more non-coding DNA than Prokaryotes?" at http://www.askabiologist.org.uk/answers/viewtopic.php?id=7816 . One biologist answered the question as follows:
Short answer there is no "junk" DNA. [I]t all has valuable functions[:] we just aren't totally sure what they are. For sure much of the DNA between genes controls their expression (spatially and temporally) - so called enhancers and promoters. Prokaryotes have far less non-coding DNA because they need small "portable" genomes which would largely prevent or at least select against non-coding DNA. The other point is that multicellular organisms need a far higher level of complexity and subtlety in gene function - thus explaining at least in part why eukaryotes have much much more "junk" DNA than prokaryotes.
It sounds like this biologist was denying the very existence of junk DNA, although he made the point that in prokaryotes, which need small portable genomes, there is stronger selection against non-coding DNA. Another cautioned:
I’m not sure that there will be absolutely no ‘junk’ DNA in genomes, but one definition of a gene as “a locatable region of genomic sequence, corresponding to a unit of inheritance, which is associated with regulatory regions, transcribed regions and/or other functional sequence regions” (Sequence Ontology consortium, 2006) points in that direction.
A third wrote:
As eukaryotes tend to have smaller population sizes, genetic drift plays a larger role, thus the preservation and accumulation of such sequences becomes more likely. This would suggest that non-coding DNA may have appeared and been preserved for non-adaptive reasons initially, but later provided benefits: roles in regulation, as an evolutionary source of new genetic information and genome complexity, etc. (see above). As most non-coding DNA is comprised of transposable elements (or sequences likely derived from them), I suspect a comprehensive answer to your question would need to invoke the reproductive mechanisms of TEs, their evolution, and the cost vs benefit to organisms of preserving vs removing them. It seems likely that prokaryotic asexuality has a role in their relative paucity of non-coding DNA, as TEs tend to flourish during DNA exchange and recombination, which occurs relatively infrequently in asexual prokaryotes. There are examples of TEs being lost in asexual eukaryotic species (e.g. retrotransposons in asexual rotifers). Nucleomorphs provide a more extreme example: genome sequencing revealed that the eukaryotic endosymbiotic nucleomorph genome in a cryptomonad cell had completely lost all its transposable elements and possessed negligible amounts of non-coding DNA.
So according to this biologist, junk DNA tends to accumulate in organisms with small population sizes, where genetic drift plays a larger role. Also, junk DNA will be preserved if it later provides indirect benefits to the organism - e.g. "in regulation, as an evolutionary source of new genetic information and genome complexity." The biologist also pointed out that prokaryotes are asexual, but added that since transposable elements (which make up most non-coding DNA) "tend to flourish during DNA exchange and recombination," there would be a reason for them to be prevalent in sexually reproducing organisms. However, in asexual eukaryotic species, transposable elements tend to get deleted. So sexual reproduction has a lot to do with it. But then I found this in a Website on onions:
When it comes to the onion, its history is different from that of a human or mouse, not only because it is by nature a plant, but also because it maintains the capacity as a true bulb plant to reproduce both sexually through flowering and asexually via producing “bulbils” or very tiny bulbs (the latter thought to be a technique used in times of hardship). Interestingly, it has been shown that mobile elements, when they are not deleterious, have a tendency to expand in number, sometimes rapidly, through asexual reproduction [2]. Because the onion has both an extremely large genome and has the capacity to reproduce asexually, this may in fact suggest that there was a very rough time in the onion’s evolutionary past which necessitated a prolonged period or periods of asexual reproduction which led to a boom in non-deleterious transposable element number and therefore an expansion in the size of its genome.
Hmm. I'm a little confused now.vjtorley
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