Basic Math Challenge: Chimpanzee and Human DNA divergence

[mark kennedy]

Another "not accounted for" difference which ups the % are the presence of the genes SRGAP2 (a, b, c, and d) which are located on three distinct parts of Chromo 1 (which in humans are critical to brain development) are nowhere present in ANY apes, chimps included! IMO this separates us from ANY ape-like ancestor (just my opinion).

They have discovered at least two dramatic giant leaps that would have had to occur in order of the human brain to have emerged from ape like ancestors SRGAP2, HAR1F. In addition genes involved with the development of language (FOXP2), changes in the musculature of the jaw (MYH16) , and limb and digit specializations (HACNS1).

The ancestral SRGAP2 protein sequence is highly constrained based on our analysis of 10 mammalian lineages. We find only a single amino-acid change between human and mouse and no changes among nonhuman primates within the first nine exons of the SRGAP2 orthologs. This is in stark contrast to the duplicate copies, which diverged from ancestral SRGAP2A less than 4 mya, but have accumulated as many as seven amino-acid replacements compared to one synonymous change. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)
​

More puzzling still, in an area known as the Human Accelerated Regions, there is this curious regulatory gene, a gene that has changed the least over just under 400 million years HAR1F. Just after the Cambrian is would have had to emerge de novo, fully formed, fully functional and permanently fixed along broad taxonomic categories. In all the time since it would allow only two substitutions, then, while the DNA around it is being completely overhauled it allows 18 substitutions in a regulatory gene only 118 nucleotides long. The vital function of this gene cannot be overstated:

The most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal– Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. (An RNA gene expressed during cortical development evolved rapidly in humans, Nature 16 August 2006)​

This all has to occur after the chimpanzee human split, while our ancestors were contemporaries in equatorial Africa, with none of the selective pressures effecting our ancestral cousins. This is in addition to no less then 60 de novo (brand new) brain related genes with no known molecular mechanism to produce them.

Very curious, very curious indeed.

 

[essentialsaltes]

They did provide a number, they provided the number of events.

Certainly. It was the same number as in the paper. No problem there.

It has nothing to do with the total number of base pairs involved but they changed the DNA that is identical to 98% to 99% which is absurd.

They said it was appropriate to describe it that way. And they proffered many other measures that might also be appropriate in different contexts that give different results.

 

[mark kennedy]

Certainly. It was the same number as in the paper. No problem there.

Except the number of events doesn't change the number of base pairs.

They said it was appropriate to describe it that way. And they proffered many other measures that might also be appropriate in different contexts that give different results.

Not when your comparing base pairs.

 

[pshun2404]

Yes the HAR1 is most interesting indeed...in simple terms related to HAR 1, when evolutionists use the word “similarity” they are using what is called a “weasel word”. Weasel words are a class of terms intentionally persuasive, but also misleading as to actual truth value. For example when we consider the HAR 1 gene, this gene is found in almost all mammals. The difference between chimps and any other mammal except humans boils down to only 1 or 2 base pairs (which they attribute to mutation but cannot show it was once something other which later became this, thus mutation as used in this sense is also a weasel word).

The truth is that the human HAR1 demonstrates the difference with Chimps you noted of 18 base pairs (and this is a gene so this makes it very different in form and function). YET...because the Chimps have a HAR 1 and Humans have a HAR 1 they count this as a similarity in most literature when doing their tallying. But in reality (not hypothesis driven) this alone constitutes a significant DIFFERENCE.

I once observed the same thing when some Critical Scholars having found an error repeated in the Western Textual tradition 300 times (a copiest error repeated by scribes that followed) reported it as 300 variants from the Majority Text in that one text type alone...yet it was actually only one variance we could actually see, AND it actually had nothing to do with the Byzantine tradition at all because it varied from the Alexandrian and the Syriac as well.

 

[mark kennedy]

Yes the HAR1 is most interesting indeed...in simple terms related to HAR 1, when evolutionists use the word “similarity” they are using what is called a “weasel word”. Weasel words are a class of terms intentionally persuasive, but also misleading as to actual truth value. For example when we consider the HAR 1 gene, this gene is found in almost all mammals. The difference between chimps and any other mammal except humans boils down to only 1 or 2 base pairs (which they attribute to mutation but cannot show it was once something other which later became this, thus mutation as used in this sense is also a weasel word).

The truth is that the human HAR1 demonstrates the difference with Chimps you noted of 18 base pairs (and this is a gene so this makes it very different in form and function). YET...because the Chimps have a HAR 1 and Humans have a HAR 1 they count this as a similarity in most literature when doing their tallying. But in reality (not hypothesis driven) this alone constitutes a significant DIFFERENCE.

I once observed the same thing when some Critical Scholars having found an error repeated in the Western Textual tradition 300 times (a copiest error repeated by scribes that followed) reported it as 300 variants from the Majority Text in that one text type alone...yet it was actually only one variance we could actually see, AND it actually had nothing to do with the Byzantine tradition at all because it varied from the Alexandrian and the Syriac as well.

Well with HAR1f there are two substitutions in better then 300 million years and then 18 since the split. That coupled with some 60 brand new brain related genes starts adding up to a major giant leap in evolution.

And yea, I've seen them do that thing with the text variation, I mean who are they kidding? There isn't a dimes worth of difference in the manuscripts, the Old Testament is even more remarkable given it's age. The thing about the Scriptures is that they have been attached to living persons their entire history, the Hebrew and Christian communities respectively. I find that so much more credible then a bunch of old bones and the age of dirt.

 

[pshun2404]

Why are they "Substitutions" since they have always been there? There has never been a human without them! And no one can show they were not in and then were in ANY alleged Common Ancestor from the alleged 3, 5, 6, 8 million years ago (they cannot pin that one down)...so in reality it is all made up, imagined, even so called "inference" is opinion based interpretation by those already "convinced" of the common ancestor hypothesis (their opinion has been shaped by appeal to authority and argumentum ad populum not by observed facts)

Now when you (and others) claim the 18 happened SINCE the split can you or any other SHOW any examples of say when there were only say 10 or 14 (since the alleged split of course)?

If not what is the basis for this claim? Why should anyone believe it is true or correct? Because some bunch of old bearded ones say so? And don't even try and demonstrate the alleged "60 brand new brain genes" accumulating...accumulating where...when...in what?

Even if there are 60 different type of levels of brains in the ancient past this does not mean one came from the other, that's the logic fallacy of false causes.

Just because a former existed before a latter does not necessitate that the latter came from or exists because of the former. DO you agree with this last statement?

 

[JDD_III]

Depends how define identicle.

In "orthological" regions (i.e. those sequences you can actually align) it is probably around 98% identical.

However there are aspects that are vastly different. For example, the Y chromosome is probably only around 68% if I recall correctly homologous to the chimp Y.

Of course evolutionists claim this is because there is little selective or purifying pressure on this chromosome...

 

[mark kennedy]

Depends how define identicle.

In "orthological" regions (i.e. those sequences you can actually align) it is probably around 98% identical.

However there are aspects that are vastly different. For example, the Y chromosome is probably only around 68% if I recall correctly homologous to the chimp Y.

Of course evolutionists claim this is because there is little selective or purifying pressure on this chromosome...

Orthologous proteins in human and chimpanzee are extremely similar, with ~29% being identical and the typical orthologue differing by only two amino acids, one per lineage. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

I'm not exactly sure but any change in the amino acid sequence is never without deleterious risks. Only 29% of proteins are identical, that makes for a lot of change.

 

[JDD_III]

Orthologous proteins in human and chimpanzee are extremely similar, with ~29% being identical and the typical orthologue differing by only two amino acids, one per lineage. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

I'm not exactly sure but any change in the amino acid sequence is never without deleterious risks. Only 29% of proteins are identical, that makes for a lot of change.

Indeed, only 29% are exactly identical which sounds low, but when you consider that of the other ~70%, on average they differ by only 2 amino acids.

If you assume there are ~20,000 genes but be generous and to account for splice variants we say the proteins are at 180,000, then 71% of this makes 127,800 proteins that could be different between the 2 species. Then, continuing to be generous lets say there is an average of 6 base pairs difference (although with a single bp you can get a different amino acid) then you have 127,800 x 6 = 766,800 bp, so just under 1million bp differences on average in protein coding regions alone (which makes up probably <2% of the genome). If the genome is 3billion bp and let’s be generous and say 2% is protein coding, then that gives us 60,000,000 bp for coding protein. So 766,800 of that is 1.28% difference.

This does not take into account synonymous mutations in the DNA, but just a “back of a [bless and do not curse][bless and do not curse][bless and do not curse] packet” calculation to illustrate the little difference in protein coding. It does also not take into account protein-coding genes that are not present in the counterpart genome, as those will obviously be 100% different (ORFan genes).

As you say, most mutations/changes in amino acids have a deleterious effect. Also, this approach does also not address the impact of such mutations on alternative reading frames that encode for proteins within the gene itself, which will be more greatly impacted potentially by mutations in the canonical reading frame. Some people (mainstream scientists) believe such alternative ORFs are highly prevalent across eukaryotic genomes.

I think the real story is not what is similar or identical in the <2% of the genome that encodes for the protein, but the very fact that chimps and humans are so different in many ways (just look at the two skeletons and you can see that). So clearly, the small difference in the 2% of the genome encoding for proteins alone is not sufficient to account for this. As some scientists including myself have been saying for many years now, there is clearly greater functionality in the “junk” regions of DNA that previously attributed to by evolutionists. The regulation of these genes is the key, and the associated RNA molecules are important. There is also a potential role for “pseudogenes” vastly underappreciated in this context.

Is it really a surprise that something that looks and acts a bit closer to humans has the most similar code to humans? Would we not think it odd if a cow’s genome was more similar to ours that a chimp’s genome? Why is similarity more evidence of naturalistic evolution than design?

 

[Tanj]

Is it really a surprise that something that looks and acts a bit closer to humans has the most similar code to humans?

Using this logic, wouldn't fish and whales have similar genomes? Or at least the whale would be close to a fish than a human

 

[pshun2404]

Using this logic, wouldn't fish and whales have similar genomes? Or at least the whale would be close to a fish than a human

Sorry Tanj I get the point but your analogy was bad. Humans to chimps would be like bass to sharks, or dolphins to whales...they are similar but this does not mean one came from the other or both came from the same source creature (though they might have).

 

[essentialsaltes]

Sorry Tanj I get the point but your analogy was bad. Humans to chimps would be like bass to sharks, or dolphins to whales...they are similar but this does not mean one came from the other or both came from the same source creature (though they might have).

Tanj has a very good point. Why do you group dolphins and whales, and not dolphins and sharks? Because you have some other knowledge about these creatures.

But your original statement was:

"Is it really a surprise that something that looks and acts a bit closer to humans has the most similar code to humans?"

So if you saw these creatures, I think you'd have to say you would expect their codes to be similar, yes?

 

[USincognito]

Another "not accounted for" difference which ups the % are the presence of the genes SRGAP2 (a, b, c, and d) which are located on three distinct parts of Chromo 1 (which in humans are critical to brain development) are nowhere present in ANY apes, chimps included! IMO this separates us from ANY ape-like ancestor (just my opinion).

Yeah, that's because it, along with ARHGAP11B, evolved long after the human lineage split with the chimpanzee lineage.

 

[mark kennedy]

Indeed, only 29% are exactly identical which sounds low, but when you consider that of the other ~70%, on average they differ by only 2 amino acids.

That's a mean average and the variation is much more significant. One amino acid difference per lineage. In the amino acid sequence of an open reading frame a single nucleotide substitution can cause major differences in the protein product, most often resulting in a frameshift mutation and a truncated protein product. The deleterious effects are extremely important to consider since the overwhelming probability is that it's functionally degenerative.

If you assume there are ~20,000 genes but be generous and to account for splice variants we say the proteins are at 180,000, then 71% of this makes 127,800 proteins that could be different between the 2 species. Then, continuing to be generous lets say there is an average of 6 base pairs difference (although with a single bp you can get a different amino acid) then you have 127,800 x 6 = 766,800 bp, so just under 1million bp differences on average in protein coding regions alone (which makes up probably <2% of the genome). If the genome is 3billion bp and let’s be generous and say 2% is protein coding, then that gives us 60,000,000 bp for coding protein. So 766,800 of that is 1.28% difference.

The only real statistic I have heard about that comes to about 40,000 changes in 20,000 genes which is exactly what we have here. The best examples are specific genes and then the mean average starts to take on a different perspective. Narrowing the focus to a specific chromosome is helpful:

Among the 231 genes associated to a canonical ORF, 179 show a coding sequence of identical length in human and chimpanzee and exhibit similar intron–exon boundaries. For those 179 genes, the average nucleotide and amino acid identity in the coding region is 99.29% and 99.18%, respectively. Of these, 39 genes show an identical amino acid sequence between human and chimpanzee. (DNA sequence and comparative analysis of chimpanzee chromosome 22, Nature 2004)​

Only 39 of the 231 genes are identical, even though the sequence identity is very close. So in practical terms:

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins).​

This does not take into account synonymous mutations in the DNA, but just a “back of a [bless and do not curse][bless and do not curse][bless and do not curse] packet” calculation to illustrate the little difference in protein coding. It does also not take into account protein-coding genes that are not present in the counterpart genome, as those will obviously be 100% different (ORFan genes).

My single biggest problem there is brain related genes, same problem with the fossil record. The human brain is nearly three times bigger then a chimpanzee, the genetic basis is telling since most of these changes would have happened about 2 mya since larger cranial capacity is unknown previously.

The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)
​

An amino acid substitution here and there is one thing but brand new genes involved in brain development is on a whole other level.

As you say, most mutations/changes in amino acids have a deleterious effect. Also, this approach does also not address the impact of such mutations on alternative reading frames that encode for proteins within the gene itself, which will be more greatly impacted potentially by mutations in the canonical reading frame. Some people (mainstream scientists) believe such alternative ORFs are highly prevalent across eukaryotic genomes.

Yea I know what you mean, there is this nylon eating bacteria. They thought it was adapted through a beneficial mutation but as it turns out, it was a swapped out open reading frame. Apparently bacteria had a cut and splice mechanism for adapting it's immune system. Once they uncovered it and learned how to use it, it became a revolutionary genetic engineering tool. It's called the CRISPR gene by the way.

(How A Gene Editing Tool Went From Labs To A Middle-School Classroom, NPR)

I think the real story is not what is similar or identical in the <2% of the genome that encodes for the protein, but the very fact that chimps and humans are so different in many ways (just look at the two skeletons and you can see that). So clearly, the small difference in the 2% of the genome encoding for proteins alone is not sufficient to account for this. As some scientists including myself have been saying for many years now, there is clearly greater functionality in the “junk” regions of DNA that previously attributed to by evolutionists. The regulation of these genes is the key, and the associated RNA molecules are important. There is also a potential role for “pseudogenes” vastly underappreciated in this context.

I've since lost track of it but I was once reading on how regulatory genes can literally be coded from any region of the DNA. I doubt seriously there is a lot of junk DNA, although pseudogenes are sometimes just broken genes, the GULO gene comes to mind. Regulatory genes and transcriptomes seem like the usual suspects.

The regulatory expressions are considerable as well:

"In the cerebral cortex, the biggest difference in gene expression is between the primary visual cortex and the anterior cingulate cortex in both humans and chimpanzees, where 193 and 227 genes differ in expression in humans and chimpanzees, respectively."(Cerebral Cortex, Vol. 12, No. 7, 671-691, July 2002)

"Only one gene out of the 4998 genes with detectable expression differs in expression between Broca's area and the left prefrontal cortex in all three humans analyzed and none in chimpanzees."

Figure 3 Number of genes exhibiting expression patterns specific to brain regions in humans and chimpanzees.​

Is it really a surprise that something that looks and acts a bit closer to humans has the most similar code to humans? Would we not think it odd if a cow’s genome was more similar to ours that a chimp’s genome? Why is similarity more evidence of naturalistic evolution than design?

It's not so much what the differences are as how they got there. I keep hearing that we are 98%-99% the same in our DNA and I know for a fact that statistic is just plain wrong. Then it's that the protein coding genes are nearly identical and that isn't true either. Then you cross reference with paleontology and start to realize the cranial capacity of our supposed ancestors were static at chimpanzee size (slightly bigger sometimes) right up until 2 mya. Since then they have discovered at least two dramatic giant leaps that would have had to occur in order of the human brain to have emerged from ape like ancestors SRGAP2, HAR1F. In addition genes involved with the development of language (FOXP2), changes in the musculature of the jaw (MYH16) , and limb and digit specializations (HACNS1).

That's a lot going on there and molecular mechanisms capable of doing something on this scale and across the genome is elusive. There's lots of room for a little skepticism here, one thing is for sure, random mutations is the worst possible explanation. Especially in highly conserved protein coding and regulatory genes, the deleterious effects would be devastating and random mutations cannot being to account for de novo genes.

Grace and peace,
Mark

 

[USincognito]

For example when we consider the HAR 1 gene

No such gene exists.

 

[JDD_III]

Using this logic, wouldn't fish and whales have similar genomes? Or at least the whale would be close to a fish than a human

This was a hyperbolic statement to make the point - in any multi-component system some things will be more alike than others. It is unsurprising when things that appear similar externally are in their parts, more similar. Not always true, but an obvious paradigm.

In other words, similarity does not prove common descent.

 

[sfs]

In other words, similarity does not prove common descent.

No, but nested similarity in elements that have nothing to do with appearance is powerful evidence for common descent. And the way the differences so strongly resemble accumulated mutations provides evidence that is even more powerful, especially when there is no alternative explanation for it.

 

[JDD_III]

That's a mean average and the variation is much more significant. One amino acid difference per lineage. In the amino acid sequence of an open reading frame a single nucleotide substitution can cause major differences in the protein product, most often resulting in a frameshift mutation and a truncated protein product. The deleterious effects are extremely important to consider since the overwhelming probability is that it's functionally degenerative.



The only real statistic I have heard about that comes to about 40,000 changes in 20,000 genes which is exactly what we have here. The best examples are specific genes and then the mean average starts to take on a different perspective. Narrowing the focus to a specific chromosome is helpful:

Among the 231 genes associated to a canonical ORF, 179 show a coding sequence of identical length in human and chimpanzee and exhibit similar intron–exon boundaries. For those 179 genes, the average nucleotide and amino acid identity in the coding region is 99.29% and 99.18%, respectively. Of these, 39 genes show an identical amino acid sequence between human and chimpanzee. (DNA sequence and comparative analysis of chimpanzee chromosome 22, Nature 2004)​

Only 39 of the 231 genes are identical, even though the sequence identity is very close. So in practical terms:

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins).​

My single biggest problem there is brain related genes, same problem with the fossil record. The human brain is nearly three times bigger then a chimpanzee, the genetic basis is telling since most of these changes would have happened about 2 mya since larger cranial capacity is unknown previously.

The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)
​

An amino acid substitution here and there is one thing but brand new genes involved in brain development is on a whole other level.



Yea I know what you mean, there is this nylon eating bacteria. They thought it was adapted through a beneficial mutation but as it turns out, it was a swapped out open reading frame. Apparently bacteria had a cut and splice mechanism for adapting it's immune system. Once they uncovered it and learned how to use it, it became a revolutionary genetic engineering tool. It's called the CRISPR gene by the way.

(How A Gene Editing Tool Went From Labs To A Middle-School Classroom, NPR)



I've since lost track of it but I was once reading on how regulatory genes can literally be coded from any region of the DNA. I doubt seriously there is a lot of junk DNA, although pseudogenes are sometimes just broken genes, the GULO gene comes to mind. Regulatory genes and transcriptomes seem like the usual suspects.

The regulatory expressions are considerable as well:

"In the cerebral cortex, the biggest difference in gene expression is between the primary visual cortex and the anterior cingulate cortex in both humans and chimpanzees, where 193 and 227 genes differ in expression in humans and chimpanzees, respectively."(Cerebral Cortex, Vol. 12, No. 7, 671-691, July 2002)

"Only one gene out of the 4998 genes with detectable expression differs in expression between Broca's area and the left prefrontal cortex in all three humans analyzed and none in chimpanzees."

Figure 3 Number of genes exhibiting expression patterns specific to brain regions in humans and chimpanzees.​

It's not so much what the differences are as how they got there. I keep hearing that we are 98%-99% the same in our DNA and I know for a fact that statistic is just plain wrong. Then it's that the protein coding genes are nearly identical and that isn't true either. Then you cross reference with paleontology and start to realize the cranial capacity of our supposed ancestors were static at chimpanzee size (slightly bigger sometimes) right up until 2 mya. Since then they have discovered at least two dramatic giant leaps that would have had to occur in order of the human brain to have emerged from ape like ancestors SRGAP2, HAR1F. In addition genes involved with the development of language (FOXP2), changes in the musculature of the jaw (MYH16) , and limb and digit specializations (HACNS1).

That's a lot going on there and molecular mechanisms capable of doing something on this scale and across the genome is elusive. There's lots of room for a little skepticism here, one thing is for sure, random mutations is the worst possible explanation. Especially in highly conserved protein coding and regulatory genes, the deleterious effects would be devastating and random mutations cannot being to account for de novo genes.

Grace and peace,
Mark

Of course it is inaccurate I was using a back of a [bless and do not curse][bless and do not curse][bless and do not curse] packet calculations littered with massive assumptions to prove a point. 29% sounds very low, but in the context of what the paper was claiming, it is not actually as low as it sounds.

Of those proteins that are shared, certainly there is generally high homology. Easy enough to do - BLAST a few human protein sequences with the chimp proteome and you will see. Now of course this may be wrong, the annotation may be wrong, the using one genome to reference the other to fill in the gaps may have happened, but my point is I believe that chimp sequences and human sequences were designed and created quite similarly. They may even have been more similar in their original design, and have deviated since the Fall. Pure speculation of course.

I actually completely agree with a lot of what you say. Another thing I find ironic is we are told cranial size and hence brain size is directly correlated with intelligence. Yet Neanderthals are said to be less intelligent hominids yet their craniums were larger than ours today. Go figure.

I still think there is much in the regulatory role of supposed "junk" DNA. When I was an undergraduate biochemist I was taught that 98% of the genome was junk. I remember reading Dawkins saying this is what we expect from wasteful evolution and opposite to design expectations. I predicted those many years ago that greater functionality would be found as I did not believe that God would design such "waste". Roll forward in time and a number of years ago extra functionality is found and the number is revised to 90% junk. Dawkins being quoted as saying "exactly as we would expect, evolution finding function for this DNA." Heads I win, tails you lose.

The regulatory role in the genome is vastly underestimated and poorly understood. Further, there are no doubt 3-dimensional features that much of this code may play, structural purposes. We now know that sequences megabases away from other genes actually are promotors and regulatory sequences of gene expression, and that the DNA bends back from far away to allow transcription to occur. Why exactly, who knows for sure, but it adds another level of complexity that we are barely scratching the surface of. Every month a new paper is published on a regulatory function for a pseudogene (hence why they look like a broken version of the gene, because they are actually complimentary binding RNAs that regulate the gene expression, not protein coding). LncRNAs, these grow by the day. We just assume we know they are functionless, out of ignorance rather than out of our arrogant assumptions we have it "figured out".

 

[sfs]

When I was an undergraduate biochemist I was taught that 98% of the genome was junk.

Where, when? I'd never heard that.

I remember reading Dawkins saying this is what we expect from wasteful evolution and opposite to design expectations.

Where did Dawkins say that 98% was the expected amount of junk DNA? Not that Dawkins has any obvious expertise in this area.

 

[Tanj]

This was a hyperbolic statement to make the point

Well I disagree, it was a cherry pick to make a point.

in any multi-component system some things will be more alike than others. It is unsurprising when things that appear similar externally are in their parts, more similar. Not always true, but an obvious paradigm.

So what you are saying is that when things that appear externally similar are internally similar thats an obvious paradigm supporting intelligent design, and when they aren't is still supports intelligent design.

Do you not see the problem with this?

By the way, there is precisely 0% of the whale genome more similar to fish that to human.