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Becoming Human: New Insights from Genome-wide Functional Genomics

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July 27, 2012 Tags: Genetics
Becoming Human: New Insights from Genome-wide Functional Genomics
Detail of Figure 4 from a recent study of changes in genetic regulatory sites (DHS’s) on the Human and Chimp genomes in different kinds of cells. Chart compares gains and losses of such sites in specific human cell lines to data from other human cell types, showing the degree of regulatory activity present at various sites of difference. Regulatory gains in the human genome relative to the chimp genome are strongly correlated the with marks of positive selection.

Today's entry was written by Dennis Venema. You can read more about what we believe here.

We live in exciting times for a geneticist: more and more genomes are being sequenced, and more and more novel genome-wide analyses are being performed to shed light on what all those newly-determined sequences mean. These genomic studies powerfully support the common ancestry of humans with other forms of life, such as chimpanzees and other great apes. These studies have also measured ancient human population size dynamics with increasingly precise methods, indicating that (biologically at least) we do not descend solely from a single ancestral couple. These topics are ones that I have commented on frequently here, since—especially in our scientifically-informed age—the church must come to terms with these important issues.

Recently, an elegant and powerful experiment was done to further investigate a question of interest to many evangelicals: how is it that we are so different from our closest biological relative (the chimpanzee) when our DNA is so very similar? Even when using estimates that maximize the differences, our genomes are 95% identical. The conclusion, that I have discussed here in the past is that a dispersed set of numerous small changes can have large effects on the form and function of an organism. Of course, small changes are what evolution specializes in: tinkering here and there, one mutation at a time, as we have directly observed in laboratory experiments. Before we discuss how this pivotal new study was done, however, a brief review of how genes work is in order.

Review: gene structure and function

If you’ve been following the ongoing Understanding Evolution series here at BioLogos, you will recall that we discussed gene structure and function not long ago, in the context of discussing non-functional DNA sequences (so-called “junk DNA”):

Genes have a typical structure (obviously simplified here somewhat). First off, there is the actual DNA sequence that specifies the protein product sequence (the so-called “coding sequence”, shown in blue). This sequence is usually broken up into segments in mammalian genes, and these sequences are spliced together when the DNA sequence of the gene is transcribed into a “working copy” called mRNA – a short duplicate of the code that can be used by the cell’s machinery to actually build the specified protein.

In addition to the actual coding sequences, other sequences are needed to tell the cell when and where certain genes should be transcribed into mRNA. Every cell in an organism has the same genes in their chromosomes, but not all are transcribed. Using different genes in different combinations is what makes cells take on distinct roles – for example, cells in your small intestine need different genes (for absorption of nutrients) than do cells of the immune system (for fighting off pathogens). Regulatory sequences make sure any given cell type has the right genes transcribed and made into protein products. Some of these sequences are part of the mRNA transcript (shown in red), and others are not transcribed but only part of the chromosomal DNA sequence (such as the “promoter” region that directs the enzymes responsible for making the mRNA transcript (shown in blue).

With this background in mind, we can now extend our understanding slightly further. DNA in cells is “packaged up” when not in use by winding it around a class of proteins called histones. This packaging keeps the DNA in a compact form, and it is useful in helping cells prevent genes they don’t need from being transcribed. For any given chromosome - which is one long strand of DNA – some regions will be packed away (and the genes there not transcribed), while other regions are unpacked (less tightly associated with histones) with the genes there actively undergoing transcription. The open regions allow for transcription because enzymes and other proteins needed for the process can gain access to the DNA there.

Comparing gene transcription across species at the genomic level

Because of the overwhelming similarity between the human and chimpanzee genomes (and the even greater similarity when examining only their protein-coding regions) it has long been hypothesized that changes in “where and when” genes are transcribed will be a major player in what makes our two species different (in contrast to the idea that we are different because of the relatively tiny changes in the coding regions of our genes). From an evolutionary point of view, there are a few ways to explore how differences in gene transcription arise once species go their separate ways, such as when our ancestors parted ways with our last common ancestor with chimps around 4-6 million years ago. The main idea is to compare the same cell type in both species: human skin cells versus chimp skin cells, for example. Determining what specific genes are transcribed (or not) in human cells and comparing the results to chimpanzee cells gives us an idea of how gene transcription differences arose in the two lineages since they last shared a common ancestor. The challenge, up until now, is that there was no easy way to indentify the changes in regulatory DNA that led to those differences in transcription. The problem arises because of the overwhelming similarities between our genomes: changes in transcription due to changes in DNA sequence are hard to find simply by looking for sequence differences, since in most cases the differences will be very small. There are also many small differences between our genomes that have no effect on gene transcription, so we cannot simply look for any difference at all. What we need is a way to identify which small changes led to differences in gene transcription.

Old hypotheses, new technology

Back in 2008, a method for addressing this issue was devised. As we have seen, DNA undergoing transcription is “unpacked” and accessible to enzymes. Researchers have long known about a certain enzyme, called DNAse I, that can cut exposed DNA but leave histone-packaged DNA alone. This means that DNA from any given cell type can be cut using this enzyme specifically at “DNAse I hypersensitive sites” (DHS’s) where regulatory DNA is unpackaged and a nearby gene is being transcribed. While this technique is decades old, what is new is a way to then go on to sequence the DNA next to each of these sites. This requires what is known as “next-generation” or “deep” DNA sequencing methods that can use a linker sequence to attach to the DNAse I cut sites and then amplify and sequence individual DNA fragments attached to the linker. Since we have the entire genome sequence of humans and chimps it is then trivial to take the sequencing results and map them to either genome. The results are a detailed map of what chromosome regions are unpacked and regulating transcription in each cell type. These maps can then be compared with related species across entire genomes.

It was only a matter of time before these powerful methods were applied to the human-chimp question, and the first results became available last month. The research group was of course interested in differences between the two species, and the results are fascinating. The researchers looked at several different cell types, and found similar results in all cases. The results for any given gene fall into one of several categories when compared to the human-chimp (H-C) last common ancestor:

  • No differences in regulatory DNA relative to the H-C last common ancestor (1259 genes)
  • Gain of regulatory DNA in humans relative to the H-C last common ancestor (836 genes)
  • Loss of regulatory DNA in humans relative to the H-C last common ancestor (286 genes)
  • Gain of regulatory DNA in chimpanzees relative to the H-C last common ancestor (676 genes)
  • Loss of regulatory DNA in chimpanzees relative to the last common ancestor (211 genes)

While it was not surprising to find a significant percentage of unchanged genes, it was interesting to note the large percentage of differences in regulatory DNA, despite the overwhelming genomic similarity between the two species. Small changes had a large impact on gene regulation. The researchers went on to examine the new regulatory regions they had identified, and found that they showed evidence of being under natural selection. These mutations had not only brought change, but provided an advantage to their hosts.

These results underscore a few important points:

  • Species become different because differences accumulate in both lineages once a common ancestral population splits into two. The differences we see in modern species are due to changes both species have accumulated over time.
  • Tweaking the regulation of numerous genes appears to be a widespread mechanism for generating evolutionary novelty. Both gaining and losing regulatory sequences is common.
  • These gains or losses in regulatory DNA require only very small changes at the DNA sequence level, but they can have profound impacts on how genes are transcribed.
  • These changes appear to be widespread in genomes, and able to accrue in short evolutionary timescales.
  • Small changes are exactly the sort of thing that evolution is known to be able to accomplish easily, one mutation at a time.
  • These small changes bear the marks of natural selection, indicating that they were selected for as they arose.
  • Anyone who wishes to call these differences “insignificant” will have to contend with the observation that the biological differences we observe between humans and chimpanzees are significant.
  • Small, incremental changes at the genomic level fit nicely with the fossil evidence for human evolution, which, though fragmentary, indicates gradual changes in skeletal morphology over the same timescale.

Of course, this study is just the beginning, and future studies are sure to examine and compare additional cell types found in humans and our evolutionary cousins. These results have already added to the troubles of antievolutionary groups that wish to portray the differences between us as too great for evolutionary mechanisms to bridge. I suspect these troubles will only worsen in the coming years as these new techniques come into their own.

For further reading:

Shibata Y, Sheffield NC, Fedrigo O, Babbitt CC, Wortham M, et al. (2012). Extensive Evolutionary Changes in Regulatory Element Activity during Human Origins Are Associated with Altered Gene Expression and Positive Selection. PLoS Genetics 8(6): e1002789. doi:10.1371/journal.pgen.1002789


Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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Eddie - #71400

July 27th 2012

Looks like the beginning of an interesting new series, Dennis.  I’ll keep my eye open for further columns on this theme.

By the way, in case you don’t look back at comments on your older columns, I wanted to note that I asked a question (70916) under this column:


If you get time to look back at that question, I’d be grateful for any references you could supply.

Dennis Venema - #71509

July 30th 2012

Hi Eddie,

Sorry, I’ve been on vacation and not around here much. Have a look at page 134-135 in Edge of Evolution.

Eddie - #71537

July 31st 2012


Thanks for this reply (71509).

I read that passage in EoE differently.  It seems to me that Behe clearly distinguishes there between mutations which, taken singly, are neutral, and mutations that, taken singly, would cause trouble.  And it seems to me that he explicitly states (p. 134) that if the mutations were neutral they would not need to occur simultaneously.  And it was neutral mutations that I asked about.

The mutations would have to occur simultaneously where they would do damage if they occurred singly.  Behe appears to believe that this is what happens in the case of chloroquine resistance.  I don’t see, however, any place where he applies this argument to neutral mutations.  Nor do I see this as a general claim of ID proponents, that neutral mutations would have to occur simultaneously.  Thus, I don’t understand your reading of this passage, and I don’t think your statement in your reply to Tony below, about simultaneous mutations, is an accurate representation of the ID position.

dennis.venema - #71554

July 31st 2012

Hi Eddie,

You’re right, Behe does not claim that neutral mutations need to be simultaneous. I have not suggested that he does claim that, so I’m a bit confused why you think I have.

The point is that Behe claims that new protein-protein binding sites cannot arise solely through neutral mutations, but that such sites require simultaneous amino acid substitutions to arise. It’s all there in EoE, Behe lays it out at length.

Eddie - #71563

August 1st 2012


Glad we have cleared that up about the neutral mutations.  I did not think I had misread Behe, but I wanted to be sure.

I would, however, appreciate short quotations and page numbers regarding the rest of your comments.  If Behe lays it out at length, as you say, you should have no problem documenting that Behe affirms that “new protein-protein binding sites cannot arise solely through neutral mutations” and that “such sites require simultaneous amino acid substitions to arise.”  I’ve read the book, but I missed direct statements of these two points.  That is why I am wondering if these statements are something that you inferred from the book rather than found directly claimed in the book.

I’m not trying to be contentious here, just trying to determine how you discerned what Behe was arguing.  If you are simply reporting what he said, then showing me the passages will answer my question.  But if you are drawing an inference, e.g., “Behe must be assuming that the amino acid substitions are simultaneous, because otherwise he wouldn’t argue X,” I’d like a few typical passages on which your inference is based.

George Bernard Murphy - #71404

July 27th 2012

Genes don’t make humans.

Paper doesn’t make books.

Books are printed on paper.

 Humans are recorded on DNA.

When we lose the DNA created bodies WE will still exist in heaven.

wesseldawn - #71413

July 28th 2012

Don’t forget though George that the reason why Jesus appeared was so that the DNA part of us might be preserved (at the resurrection):

But we are not of them who draw back unto perdition; but of them that believe to the saving of the soul. (Heb. 10:39)

Darwin Guy Dan - #71521

July 31st 2012

James A. Shapiro wrote a book.  The title of Shapiro’s book is an advertising  hook.  Yes, of course, the title rhymes with “solution.” 

But while common ancestry is false and thus false is “Evolution,”  Shapiro’s marvelous book itself is a book for future history.  The book’s subtitle is “A View From the 21st Century.”

Shapiro’s book is NaturalHistoryGuy’s book of the year for 2012, Always nearby and ready to deshelve. 

George Bernard Murphy, just exactly where is “heaven”?  I can tell you that Shapiro’s book was published in 2011.

Shall we work to make it in heaven like it is on Earth?   Or shall that have to wait for some sort of rebirth? 

Will we get to the Moon again soon?  I’m not Darth Vader.  But nevertheless, one sure would like a space elevator.

Shapiro also says that a read / write disk is a metaphor for the genome.  Will planet Earth always be heaven’s home?


Stan Salthe, has an interesting definition in his book.  “The irreversible accumulation of historical information” is Salthe’s special nook.

Yes, that is Salthe’s definition of “evolution.”  Obviously we need a word revolution.

To my mind, such definitional confusion leads to delusion and is no solution.  I very much like Salthe’s idea.  But don’t you think that for a new and distinct thought, a new word ought to be sought?

“Change over time” is also just fine.  But why would the late Lynn Margulis for evolution so define?  Margulis is also author of THE SYMBIOTIC PLANET: A NEW LOOK AT EVOLUTION, published in 1999.  (Take a look.  On this subject, Margulis is a Saint in my book.) 

Louise Agassiz long ago called for standards in science.  Would that not make for far better heuristic teaching compliance (and reliance)? In 1857 Agassiz wrote his ESSAY ON CLASSIFICATION.  Any book like that will naturally leave some matters to the imagination.

But then, just precisely what is teology?  Is teology also theology?

Darwin Guy Dan - #71408

July 28th 2012

Dennis Venema,

As far as I can determine, your epistemology pretty much mimics that of the Biblicists.  Am I correct on this?  I.e., you have been correlating what Evolutionists label “the fact of Evolution”, i.e., common ancestry, with genomes and morphologies (such as those of apes and humans).  Meanwhile, Biblicists have analogously been correlating natural history with the Bible creation myths.  (Gerald Schroeder of M.I.T. also does an interesting job of this in his THE SCIENCE OF GOD: THE COVERGENCE OF SCIENTIFIC AND BIBLICAL WISDOM, 1997—- more into cosmology, Earth history, etc. than genomics.)

But aren’t we all a little old for mythology?  Do we really need the millions (or billions?) of mythological, unidentified, unnamed common ancestors that Evolution hypothesizes?

Tony Jelsma - #71411

July 28th 2012


This is an intriguing and elegant study. I have two comments about your interpretation of the paper.

You argue that these many changes account for the significant differences in morphology (and I presume behavior) between humans and chimpanzees. However, it’s one thing to show the differences; showing how they result in phenotypic changes is quite another matter, particularly since there seems to be no commonality in the gene ontology of the differentially expressed genes. After all, how would changes in gene expression in fibroblasts or lymphoblasts (or any of these cell lines) result in morphological changes in the organism? Maybe I’m asking too much of what is already a large piece of work but I would also caution against making premature extrapolations of the data.

Moreover, such an interpretation is in striking contrast to the prevailing view in evo-devo that evolutionary changes are caused by changes in expression of a relatively small set of developmental genes. Do you see a conflict between that understanding and this particular study?

Dennis Venema - #71510

July 30th 2012

Hi Tony,

Can you explain what you mean by “no commonality in the gene ontology of the differentially expressed genes”? I don’t think I understand what you’re indicating here.

As for your question about evo-devo, that’s more about major differences in body plans. Chimps and humans are built on the same basic (mammalian, primate) body plan, so I wouldn’t expect much in terms of large differences in early developmental genes (with the exception of brain development, perhaps).


Tony Jelsma - #71516

July 30th 2012

I’m referring to the bottom of page 6 (of the pdf), left column:

We conducted gene ontology enrichment analysis for both
species-specific DHS sites using GREAT [34] and differentially
expressed genes using GO (http://david.abcc.ncifcrf.gov/), but
did not find many highly enriched categories in either analysis
(Table S9). This indicates that chromatin gains and losses occur
near many different types of unrelated genes representing a broad
spectrum of gene ontologies.

Do you think that chimp fibroblasts are functionally different from human fibroblasts and that this might contribute to differences in chimp vs. human connective tissue? How would human connective tissue be different from that of chimps?

It is my understanding that even minor morphological differences are due to differences in the expression of developmental genes e.g. the role of BMP4 in beak length.

dennis.venema - #71535

July 31st 2012

Thanks Tony, I understand what you are asking now. The authors were interested to see if any specific categories of genes were differentially selected for these small changes. They found that the changes were distributed across genes of many different types, and not clustered in a few types. This is in keeping with the hypothesis that the differences we see between humans and chimps are the result of numerous small changes, not a few large ones. 

This finding undermines the ID assertion that humans and chimps are too genetically different for natural mechanisms to bridge. We don’t see major changes that require multiple simultaneous mutations. We see numerous small changes that combine to shift gene expression patterns. 

Note too that the signature of selection is genomic, and not necessarily because of a given gene’s expression in the various cell types. These genes are almost certainly plieotropic in their function, so the selection is probably due to expression in other cell types (though in principle it could include fibroblasts as well). 

As for the comparision between human and chimp fibroblasts, I expect they would be pretty similar. It seems that tweaking/shifting the expression profile of a set of genes does not impede fibroblast function, and if indeed some of the selection was due to expression in fibroblasts, perhaps improved its function relative to other changes that were selected in other cell types. 

I admit I can’t quite recall your stance on human evolution, though I know you advocate some form of ID. Could you remind me if you accept or reject common ancestry? That might help me see where you are coming from.

Thanks for the questions,


Tony Jelsma - #71551

July 31st 2012

Dennis, you said,

“Note too that the signature of selection is genomic, and not necessarily because of a given gene’s expression in the various cell types. These genes are almost certainly plieotropic in their function, so the selection is probably due to expression in other cell types (though in principle it could include fibroblasts as well).”

 Except the authors state (left column p4), citing Figure 4a, “…that DHS gains are largely cell-type specific.” They continue (left column bottom p9), stating that DHS changes are cell-type specific i.e. these changes in expression are predominately not pleiotropic.

 I acknowledge the high similarity between the human and chimpanzee genomes, including synteny, shared pseudogenes and repeat sequences, as a strong argument for common ancestry. I’m somewhat skeptical of the ability of natural selection to accomplish the myriad changes between humans and chimps in such a geologically short period of time. Given the robustness of gene regulatory networks to perturbation, I’m not convinced that tweaking a bunch of genes in differentiated cell types can account for the differences in morphology and function between humans and chimps.

 Moreover, what you seem to be advocating is exactly what Darwin was proposing (minus the molecular biology of course), whereas this is generally acknowledged to be inconsistent with the fossil record and the prevailing models of evo-devo.

dennis.venema - #71555

July 31st 2012

Hi Tony,

They’re “cell type specific” when compared to the handful of cell types examined in the paper, not the totality of possible cell types in humans or chimpanzees. It would be pretty unusual for all those genes to be restricted to expression only in one cell type, or for their expression to be altered only in one cell type. 

As for the “myriad changes” you reference, I’d be curious to know which specific ones you think are beyond the reach of natural mechanisms, and why. I posed the same question to Douglas Axe years ago, but have yet to see a reply. The challenge, of course, is the overwhelming similarities between the two genomes. 

Tony Jelsma - #71571

August 1st 2012

>They’re “cell type specific” when compared to the handful of cell types examined in the paper, not the totality of possible cell types in humans or chimpanzees. It would be pretty unusual for all those genes to be restricted to expression only in one cell type, or for their expression to be altered only in one cell type.

From the bottom of p9, left column, “Most regulatory element changes occurred within intergenic regions and introns and were predominantly associated with cell type-specific DHS sites. These results are consistent with expected differences in the extent of pleiotropy: loss of core promoter elements will more likely affect transcription in many tissues and stages of development, while loss of distal enhancers will more likely affect transcription in a subset of tissues. Lower rates of change in core promoter elements and in regulatory elements actively utilized in multiple tissues suggest negative selection is operating to maintain regulatory elements with more critical functions.” The point they’re making here is that the predominant changes were not pleiotropic (didn’t I already say that?). Where changes were found in genes that are expressed in multiple tissues, the enhancers that were changed tended to be tissue-specific.

>As for the “myriad changes” you reference, I’d be curious to know which specific ones you think are beyond the reach of natural mechanisms, and why. I posed the same question to Douglas Axe years ago, but have yet to see a reply. The challenge, of course, is the overwhelming similarities between the two genomes. 

Don’t try to string me along here Dennis. It’s not that I think particular ones are beyond the reach of natural mechanisms; it’s the number of them. It’s pretty obvious that chimps and humans are quite different, despite their highly similar genomes. Their body plans may be somewhat similar but they are quite distinct. As I alluded to earlier, gene regulatory networks provide checks to ensure that the basic body plan will develop despite minor perturbations in development. The range of body plans of humans and chimps do not overlap. Moreover, natural selection is limited in its ability to accomplish change: too strong a selective force and the population dies out; too weak a selective force and new variants can’t overcome loss by genetic drift.

I cannot continue this discussion but let me say a few things in closing. This is an interesting paper that uses an elegant technique and careful analysis to examine how humans and chimps are different. Such a paper wouldn’t have been possible just a few short years ago. Thanks for bringing it up and stimulating new discussion. I’m looking forward to seeing how the evo-devo community addresses this paper since it differs from the predominate view of evo-devo. But as to whether it provides slam-dunk evidence for the mechanism of the evolution of humans from an ape-like ancestor, I’ll withhold judgment for now.

wesseldawn - #71414

July 28th 2012

Thank you for this very good article Dennis. I would be interested in hearing how you personally reconcile your genome studies with your faith, assuming that you are an Evangelical Christian (I.D.).

Dennis Venema - #71512

July 30th 2012

Hi wesseldawn,

I believe that “the earth is the Lord’s, and everything in it”. I see science as a (God-given) activity to understand the mechanics of His created world.

wesseldawn - #71806

August 8th 2012


Sorry, I was away. May I ask how you reconcile the first man and evolution? I’m not trying to be difficult, it’s just that I have yet to meet someone that can reasonably explain it. In my mind the only answer can be (of course I got the idea from the Bible itself) that the first man (soul=animal principle only) had to have been a primate!

PNG - #71558

July 31st 2012

You can see a more extended account by Dennis of how he came to his present views in an essay elsewhere on this site.   http://biologos.org/uploads/projects/venema_id_to_biologos.pdf

wesseldawn - #71415

July 28th 2012

I might also add that the differences between chimps and humans are ‘huge’ (in some ways as we have a tail bone) because according to the Bible, we/Adam gained a supernatural component, whereas the other animals did not! Therefore, genome studies would be limited in that respect because they could only measure ‘physical’ characteristics!


Francis - #71423

July 28th 2012

“Of course, small changes are what evolution specializes in: tinkering here and there, one mutation at a time ... These mutations had not only brought change, but provided an advantage to their hosts. … Small changes are exactly the sort of thing that evolution is known to be able to accomplish easily, one mutation at a time …”

I noticed a recent news story that focused on the same word – “mutation”.

“A genetic mutation appears to be behind some cases of a common and aggressive brain cancer, researchers at Columbia University said, and targeting the abnormality with a drug prolonged the lives of mice with the condition.” http://online.wsj.com/article/SB10000872396390444840104577551361806274348.html?KEYWORDS=mutation

Evolution depends entirely on mutations [“natural selection” just means an unpredictable (or at least extremely fallibly predictable) way of some mutations carrying on]. These mutations must be advantageous. I would think you’d need many many millions (probably billions/trillions) to yield the great panoply of life as we know it.

Yet, I can’t recall ever reading about an advantageous mutation.

I’ve read of bacteria “developing” a resistance to antibiotics. But I also read that this results from a loss of DNA information/capability. An analogy of handcuffs and henchman was given: The handcuffs are like the antibiotic which constrains the henchman’s bacterial dirty work. Unless the henchman looses an arm. Then, the handcuffs can’t stop him. He’s “free”!  (And the bacteria is still bacteria.)

Question: If you were a henchman, which would you rather be over the long-term: two-armed or one-armed?


Ed - #71515

July 30th 2012

Yet, I can’t recall ever reading about an advantageous mutation.


Perhaps you should try reading some science, or just searching Google.  Here is a recent human mutation that seems to confer resistance to HIV and other viruses.  



Its just a single paper, so I am not necessarily convinced that its a “beneficial mutation”.  But that point is that you say you cant recall, but I can find something in humans in less than 45 seconds.  The point is that there is a ton of research going on in many species, all supporting the consensus that mutations can occasionally be adaptive.  But you have to actually read.

Cornelius Hunter - #71436

July 28th 2012

Shibata, et. al. are working within what philosophers sometimes refer to as “normal” science. That is, evolution is taken as a given from the beginning. Therefore their findings, such as their evidence of positive selection in the human genome, it is not independent evidence for evolution or common ancestry. Rather, it entails the assumption that evolution occurred.

In fact, if the assumption of evolution were removed then there would be little support for it merely from the science. Rather, evolution would be a rather heroic conclusion. Therefore Dr. Venema’s warning that “the church must come to terms” with such findings is misguided.

Dunemeister - #71446

July 29th 2012

This represents a gross misunderstanding of the idea of normal science. Although evolution is a given (that is, its truth is not in doubt), the details of how it works is certainly up for grabs. In a period of normal science, a theory continues to hold so long as it provides the most useful framework for predicting and explaining outcomes. Should the problems begin to outweigh the benefits (and there are always problems, even in the hard sciences), scientists will be forced to look for alternatives. The new theory, once proposed, would be the occasion for both celebration and scorn, but if it truly does the job better than the old model, it will win over critics eventually. That is what evolution has done. And it did so because the evidence supported it and because evolutionary frameworks made better sense of the data (and actually, those amount to the same thing).

Cornelius Hunter - #71447

July 29th 2012

It is unclear what is the “gross misunderstanding” you believe you have located. Yes, evolutionists certainly do believe evolution is true and that its truth is not in doubt. But that, nor any of your other observations, changes the fact that when conclusions are also premises the reasoning is circular. Therefore Dr. Venema’s warning is misguided.

Francis - #71449

July 29th 2012

“Although evolution is a given (that is, its truth is not in doubt), the details of how it works is certainly up for grabs.”

I’m going to edit with some literary license:

Although the creation of the universe 6,000 years ago is a given (that is, its truth is not in doubt), the details of why the standard cosmological model and radiometric dating methods give wildly inaccurate measures of time is certainly up for grabs.


I’ll continue:

“[evolution] provides the most useful framework for predicting and explaining outcomes.”

Evolution is the ONLY existing framework (other than creationism) for predicting and explaining outcomes.

 [Editor’s note: Being the ONLY framework doesn’t mean you have a valid or true framework.]


“scientists will be forced to look for alternatives”

Evolutionary biologists and evolutionary scientists will NEVER look for alternatives.

Francis - #71519

July 30th 2012


You admonished me with “Perhaps you should try reading some science, or just searching Google … But you have to actually read.”

Oh, I read.

The first thing I read was your summary of the linked article:

“Here is a recent human mutation that SEEMS to confer resistance to HIV and other viruses… I am not necessarily convinced that its a “beneficial mutation”… supporting the consensus that mutations can occasionally be adaptive.”

After that enthusiastic endorsement, I clicked on the link.

And I read some more:

“The C-C chemokine receptor 5, 32 base-pair deletion (CCR5-D32) allele confers strong resistance to infection by the AIDS virus HIV.”

My first thought: Why hasn’t this “headline” been plastered over every newspaper’s front page, the Nobel Prize awarded to the authors, and massive government funding released to allow full speed ahead on this work?

My second and related thought was why isn’t “C-C chemokine receptor 5, 32 base-pair deletion” on the tip of everyone’s tongue?

I read some more:

“While such results can not rule out the possibility that some selection may have occurred at C-C chemokine receptor 5 (CCR5), they imply that the pattern of genetic variation seen at CCR5-D32 is consistent with neutral evolution. More broadly, the results have general implications for the design of future studies to detect the signs of positive selection in the human genome.”

Powerful stuff.


Ed, would you do me a favor? Would you spend another 45 seconds and show me another example of something neither you nor the researchers are necessarily convinced is a beneficial mutation? Better yet, take 90 seconds and give me two?



I’m not really that difficult. You can take a little more time, if needed.



Please make sure you “actually read” the next examples you’ll be posting shortly.  

Francis - #71599

August 1st 2012

Dennis Venema,

Could you assist Ed? Two days have passed and I haven’t received a response regarding beneficial/advantageous mutations.

I’m not asking for the impossible here. I realize we’ve never observed in nature a mutation producing a new type of organism nor have we been able to artificially induce such in a lab.

I’m just asking for two unambiguous examples of beneficial/advantageous mutations, which I’ll define as mutations increasing genetic information/capability resulting in expanded form and function. (Antibiotic-resistant bacteria don’t count, as I explained above.)

Certainly many advantageous examples must exist, because billions/trillions of them were required to yield the tremendous diversity of life on earth.

And evolution is happening all the time, I’m told. Time (i.e. needing lots of time) shouldn’t be a problem - today is a billion years from a billion years ago. Now is the time. Today is the day the Lord has made for evolution; let us rejoice and be glad in it.

Can you help?

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