Common Descent Cladograms are all Fake, Convergent Evolution Explains Everything

Like i have said n no: of times, genetic analysis assumes common ancestry. So if common ancestry is possible, then if genes are similar, they are labelled as homologs.
If not, they are thought to arise from vconvergence. There is no sure fire way to test whether this is actually true.let me quote:

So how can one decide what family a given protein belongs to? Sequence analysis aims at finding important sequence similarities that would allow one to infer homology. The latter term is extensively used in scientific literature, often without a clear understanding of its meaning, which is simply common origin. Since the mid-19th century, zoologists and botanists have learned to make a distinction between homologous organs (e.g. bat’s wing and human’s hand) and similar (analogous) organs (e.g. bat’s wing and butterfly’s wing). Homologous organs are not necessarily similar (at least the similarity may not be obvious); similar organs are not necessarily homologous. For some reason, this simple concept tends to get extremely muddled when applied to protein and DNA sequences [695]. Phrases like “sequence (structural) homology”, “high homology”, “significant homology”, or even “35% homology” are as common, even in top scientific journals, as they are absurd, considering the above definition. “Sequence homology” is particularly pervasive, having found its way even into the NLM’s Medical Subject Heading (MeSH) system. It has been assigned as a keyword to more than 80,000 papers in MEDLINE, including, to the embarrassment of the authors, most of their own. In all of the above cases, the term “homology” is used basically as a glorified substitute for “sequence (or structural) similarity”.
All this misuse of “homology”, in principle, could be dismissed as an inconsequential semantic problem. One could even suggest that, after all, since it so happened that in molecular biology literature “homology” has been often used to designate quantifiable similarity between sequences (or, less often, structures), the term should be redefined, legitimizing this usage. We believe, however, that the notion of homology is of major fundamental and practical importance and, on this occasion, semantics matters. In our opinion, misuse of the term ‘homology’ has the potential of washing out the meaning of the very concept of common evolutionary descent [695].
A conclusion that two (or more) genes or proteins are homologous is a conjecture, not an experimental fact. We would be able to know for a fact that genes are homologous only if we could directly explore their common ancestor and all intermediate forms. Since there is no fossil record of these extinct forms, a decision on homology between genes has to be made on the basis of the similarity between them, the only observable variable that can be expressed numerically and correlated with probability. The higher the similarity between two sequences, the lower the probability that they have originated independently of each other and became similar merely by chance (see 4.2). Indeed, if we take two sequences of 100 amino acid residues each that have, say, 80% identical residues, we can calculate the probability of this occurring by chance, find that it is so low that such an event is extremely unlikely to have happened in the last 5 billion years, and conclude that the sequences in question must be homologous (share a common ancestry).

Why is sequence and structural similarity considered to be evidence of homology (common origin) in the first place? Once we are confident that a particular similarity is not spurious, but rather, according to the above criteria, represents certain biological reality, is common ancestry the only explanation? The answer is: no, a logically consistent alternative does exist and involves convergence from unrelated sequences
The functional convergence hypothesis would posit that sequence and structural similarities between proteins are observed because the shared features are strictly required for these proteins to perform their identical or similar functions.Functional convergence per se is an undeniable reality. In the broadest sense, convergence is observed, for example, between all proteins that contain disulfide bonds stabilizing their structure or between all enzymes that have the same catalytic residues (e.g. a constellation of histidines and aspartates). Even more prominent motifs associated with catalytic residues are found within different structural context and, in all likelihood, have evolved convergently [722,724]. In the case of disulfide-bonded domains, convergence can even fool sequence comparison programs, translating into statistically significant (albeit not overwhelming) sequence similarity. A rather dramatic manifestation of convergence is the recent description of a “homologous” disulfide-bonded domain in Wnt proteins and phospholipase A2 [699], which was later recognized as “mistaken identity”, on the grounds of structural implausibility [77]. The classic work of Alan Wilson and colleagues comparing lysozymes from ruminants, langur monkeys, and leaf-eating birds is a textbook case that reveals the nature and extent of convergence in enzymes [471,806,816]. These studies have shown beyond doubt that several amino acid residues required for functioning in the stomach have evolved independently (convergently) in different lineages of lysozymes. Importantly, however, this set of convergent positions consists of only seven amino acid residues, a small subset of the residues that comprises the lysozyme molecule.
Source:Evolutionary Concept in Genetics and Genomics - Sequence - Evolution - Function - NCBI Bookshelf
In conclusion, two genes have a common ancestro when they share statistically significant similarity… unless of course they dont have a common ancestor. In which case, the similarity is due to convergent evolution.

i.e as far as genetics vis a vis common ancestry is concerned. Genetic similarity is a tautology. Ca is shown by similarity… Ca is shown by less similar genes… And Similar genes might not share a CA…
If its a coin toss experiment, it would go like this. If its head: CA happened.
If you get Tails: Then also CA happened.
If the coin didnt fall down… CA happened.

Edit: @Bill_II, @AMWolfe, @gbrooks9, @T.j_Runyon, @T_aquaticus, @Mervin_Bitikofer
So i dont have to repeat all this again.

Reality has a way of poking through our chosen lenses if those lenses are so wrong about things - especially when our lens is so widely shared among so many who continue to probe into that reality (i.e. – the opposite of isolationism). This is why those who wear the lens of a “young earth” (I know --that does not include you) have not been able to maintain that lens, except among their own isolated groups. And yet there was a day when everybody thought that way – the lens should have been invulnerable to any falsification on your reading of how this works. It wasn’t. There were just too many places reality did not conform for that lens to remain viable.

It may well be true that much of biology presupposes C.A. today in order to build toward other conclusions, just as astronomers [now] presuppose that the earth moves around the sun. They do so because it continues to work and be fruitful for more detailed understandings.

Here is the situation I’ve been observing (and not just with you but with how these exchanges have gone without any exception that I can think of): scientists have been building an edifice – always incomplete of course, but slowly adding things to it. Some members fall off or don’t last. Other members do last, and yet the edifice while impressive always has more needing to be done. Challengers like yourself to certain [now foundational] parts of this edifice come along and attempt to point out problems with it. And many times these alleged problems aren’t really problems at all but have been amply answered. Other times you may be correct that something just “isn’t there” yet --maybe there is a certain type of fossil that actually does still remain to be found. But here is the general observation that interests me.

These exchanges have this one commonality if we see this as a conversation between the “builders” (scientists) and the “critics” (in this case you).

Critic: “Your house has problems X, Y, and Z – the foundation must be bad.”

Builder: … explains why X, Y, and Z either have already been thought of and answered … or else we expect they soon will be. …“and besides, here is our standing house, such as it is thus far. Can you, Mr. Critic, offer a better working foundation for us to try?”

Critic (ignoring the last question): “No – but you don’t understand. If your foundation was really valid, then X, Y, and Z would not be problems for you. You’re just using a presuppositional lens that causes you to ignore these problems.”

Builder: “Well, X and Y aren’t really problems. As we keep telling you, X is just a dishonest misreading of this literature, Y has been amply answered, and Z is still an interesting matter of investigation. Besides, if our foundation is so problematic, why is there this standing house here?”

Critic: (Ignoring the last question) “Of course you think you’ve answered X and Y because you go into your investigations assuming your foundation works. And you still haven’t answered Z, and for that matter a,b,c, and d.” (still missing upper stories of the house that aren’t complete.)

Builder: “Well, I guess you’re entitled to think that way. But if our foundation is so untenable, you still haven’t explained how we already have so much of this successfully standing house here before us.”

Critic (wishing he could just ignore this singular challenge) “But it isn’t successfully standing! It’s been falling over and is about to crumble at any moment!”

Builder: “Well, you and a lot of variously motivated others have sure been trying your hardest to knock it over! For something you allege to be so fragile, one would think we would all need to be tiptoeing around lest it fall. You’ve been far from alone in stomping all over this foundation. Other than a few problematic parts that have now been culled away, the core still looks to be solid. The house is … still standing after all.”

This is how all these exchanges always go, pretty much without exception. One side declares that it doesn’t work. The other side patiently and educationally explains exactly why it can and does [or plausibly could] work. The education and growth of understanding is disproportionately present on the latter side, while the former side’s main [only?] contribution is to attempt to cast doubt. This, more than anything else, is what persuades me that the ideological critics have so far failed to be compelling.

[with edits]


@Ashwin_s I don’t want to have to go back through your 88 posts so let me just ask you straight up, What is your position? It appears to be Old Earth/ID/progressive creation. Am I correct?

The reason I ask is I don’t understand why someone who affirms ID would argue against Common Ancestry. After all Common Ancestry could be called Common Design.

Hi Mervin,

If the house you are referring to is the tree of life, it’s full of imaginary creatures at its node.i.e-The alleged common ancestor.
It’s a strange creature in the evolutionary tree… sometimes real, sometimes imaginary… when scientists make stories/hypothesis etc ,they are real creatures with real traits… however when it comes to actually identifying them… They are imaginary, non existent constructs.
It’s like showing a couple of doors, windows, and a very small no: of bricks lying on the floor and claiming it’s a house.

As to astronomers assuming the earth revolves around the sun… There is real physical evidence for the sun and the earth(The only assumption involved is that reality is real). Its a real time measurement.The Common ancestor is a much more elusive animal…
Even in evolutionary terms it’s real as well as imaginary.
And you can’t really falsify Such a creature. Nothing to test against!

For example: to verify whether genetic predictions of lineage are true. We need the genetic sequences of the common ancestors/intermediate species… How do you verify something like that?

But what we can ask ourselves is: “What would we expect to see, if this immensely long history of life and death is true?” Of all the millions of species through history, what percentage of those could we expect to be found and catalogued? Given that so many of them would be destroyed without leaving fossil trace, and given that we can only search a tiny percentage of the earth’s surface, it is pretty impressive to me that we have as many as we do.

As to “the common ancestor” – I take it that you are referring to the one trunk of the tree at the very beginning. You realize this butts up against abiogenesis, don’t you? It would be impressive indeed if we had solved those mysteries all the way back to what that must have looked like. It’s being worked on, to be sure. But beyond knowing that it was something “simple” (like a single-celled organism) or something that had reproductive capability (and granted – that is far from simple as we can now see), this is still a mystery. And that it is so does not really surprise us.

One thing I did not mean to decry in my imagined “conversation” of the last post is skepticism or criticism, even though it was cast in an almost consistently negative light there. The skeptics and critics, whatever their motivations (ideological or not) are a valuable part of the whole process. And in the past they have sometimes prevailed over long-standing edifices (like geocentrism).

In my archetypal conversation, my own pointed criticism is aimed at the critics who, because their ideological motivation is so strong, even lapse into self-deception over matters that have reasonably been addressed. And in turn they deceive others with mistaken appraisals over the true state of affairs.

One difference I see between today’s scientific “edifice” (whether it be an impressive multi-storied building or a humble few scattered bricks as you suggest) is that skeptics today (unlike back in geo-stationary times) have much more powerful tools with which to challenge potentially weak foundations. Courtesy of well-developed scientific methodologies, today’s critics have jack-hammers whereas many centuries ago, they had little more than sticks comparatively speaking. And those were only in the hands of a tiny few who had the luxurious leisure to go poking around at such things. That they managed to topple long-standing assumptions was an impressive and hard-won feat. In contrast, anything that survives today’s skeptics with their scientific and communication tools has to be impressive in its own right.

1 Like

No it doesn’t. Not one bit. It is a testable idea. For example, this paper which was discussed extensively over in the recent ERV thread found that the class of retroviruses were inserted exogenously (i.e. the genome was bombarded by viruses so to speak) as opposed to through common descent. Some of their reasons were related to the fact that less than 5% of the viral insertions were at homologous spots in the genome. What we see with common descent is 99.9%+ of viral insertions at homologous spots in the genome as is the case with humans and chimpanzees. The notion of common descent is NOT assumed but is TESTABLE.

I’ve also said this before: genes are much much much much more similar than they need to be if common descent is false. I shared a snippet of 90 base pairs that had over 53 million ways they could be arranged and have the exact same function!!! I think that we should start with some basics again for how anyone tests common descent from any genetic analysis through this useful analogy of how we read and analyze ancient texts:

No. No. and No. How about this analogy instead.

If its a coin toss experiment, it would go like this:
If it’s heads: God supernaturally intervened and we will have no natural explanation ever.
If its tails: God supernaturally intervened and we will have no natural explanation ever.
If the coin didn’t fall down: God supernaturally intervened and we will have no natural explanation ever.

Also, it appears you are quoting from: Evolutionary Concept in Genetics and Genomics - Sequence - Evolution - Function - NCBI Bookshelf

You quote mined the authors. It is interesting that you didn’t quote this part:
This view of evolution is clearly inferior to the alternative, whereby all significant similarities observed within a class of proteins are interpreted within a single theoretical framework of divergence from an ultimate common ancestor.


The first thing to do is to compare the function of an organ in two species, and also look to see if the organ has adaptations that have been selected for. Obviously, the limbs of a tetrapod are adapted to movement on land, so that is why they are not vestigial fins. They are adapted fins. The human caecum has nearly disappeared, and the main part that remains is the appendix. The human caecum has not kept the same function as seen in ancestral populations, and there has been no selection for an equally vital and different function. What is left is a rather rudimentary and non-vital function of housing some gut flora that may help to repopulate the gut at a later date which is tiny function compared to the function of digesting cellulose in other species. It is entirely possible that mutations to the caecum will add important function in the future, which is why the caecum can enlarge and shrink through time in a lineage.

Part of the confusion is that there are really two arguments when it comes to vestigial organs. The first argument is an aesthetic one. Why would a creator include such a kludgy organ in the design of an organism? If whales were created as whales, why include all this stuff from terrestrial mammals, like a vestigial pelvis for walking on land?

The second and non-arbitrary (i.e. scientific) argument is a phylogenetic one. These organs follow the expected phylogenty. We find vestial mammal features in whales because they descended from terrestrial mammals. We don’t find vestigial bird features in whales, as an example. Whether these vestigial organs turn out to be important or not, it really doesn’t matter. The evidence is the phylogeny, not our judgement of how useful they are.


That is absolutely false. Computational phylogenetics is able to test proposed evolutionary trees.

“Computational phylogenetics is the application of computational algorithms, methods, and programs to phylogenetic analyses. The goal is to assemble a phylogenetic tree representing a hypothesis about the evolutionary ancestry of a set of genes, species, or other taxa.”
Computational Phylogenetics–Wiki

If you construct a tree and randomly disperse traits throughout the tree then the algorithms used in these tests will tell you that there is no statistically significant phylogenetic signal. These trees aren’t assumed. These trees are tested as a hypothesis, and they can be falsified.

That is wrong. Let me repeat. THAT IS WRONG.

If a mouse and a jellyfish shared a gene with 100% sequence similarity, and no other mammal or vertebrate had a gene with similar sequence, then this would falsify evolution.

Again, it is the PATTERN of similarity that evidences common ancestry and evolution, not simply similarity. That pattern can be tested, and it isn’t assumed. That pattern is a nested hierarchy, or otherwise known as a phylogenetic signal.

Can you tell us why this is a bad conclusion?

Only a tiny percentage of most eukaryotic genomes are functional, and only those parts can be affected by the mechanisms you have highlighted. Most of those genomes are non-functional and they change through genetic drift. We get the same phylogenies when we compare non-functional DNA which means that the arguments you are making fall flat on their face.

1 Like

The reason I didn’t quote that was because I don’t hold to the world view that the only two options are common ancestry or separate ancestry.
The fact that common descent is more probable than separate descent (which it should be) does not make common descent true.(Besides, the fact that I shared the link should tell you that there is no intention to quote mine or pull a quick one).
And how does this change the fact that at least the author of the book admits that we can’t really prove hypotheses of common descent through genetics without the genome of related common ancestors?
These are all probability analysis based on an assumption of common descent. Its relative probability, which means that it says one species is closer than another in terms of having more similar genes in the area compared.

First off, it’s a very interesting paper.
As per the paper, 95.8% of the ERVs were found in “non-orthologous” regions…i.e they did not mess up any “functioning” genes and lead to diseases, that would cause these genes to be selected against and lost…
Other reasons are -
a) Faster than expected divergence (i.e some amount of novelty difficult to explain by plain mutation and inheritance has happened in the common ancestor).
b) The genes which “express” themselves transcript differently in humans and chimps (i.e no inheritance of function).Indicating some kind of co-option.
Ortholog genes usually denote genes with function which have been inherited. If common descent is true, this should be the vast majority of the human genome that has function.(because mutations leading to novelty in function is rare… and evolution is a step by step process).

There are papers which put the of the human genome with function and subject to natural selection between 8.2 to 10 percentage. Others put the percentage at max 25 based on “mutational load”…
And of course ENCODE famously put the no: at 80%.
Another interesting feature is a recent study on the yeast cell (representing a billion plus years of “evolution”) which found that the percentage of genes with identifiable function in yeast is 90% (That’s a rise from 30%). They basically sequentially knocked out 3 gene pairs from the yeast cell, and measured for fitness variation… Turns out 90% has a function.

We should not get anything near that with human beings…
However, If they do find 80+% of the human genome has function, then we will have to find an answer to how come the ERVs ended up bonding to functional DNA and not get selected against…

And if functions are found for most of the ERVs, we will have to explain the probability of the right genetic code ending up in the right place in the right time so often…

I expect future findings to continue proving that the human genome has function… And that ERVs also have function…

So yes, a high percentage of function for the genome should falsify evolution. (At least I think so).
And it’s encouraging to see biologists conduct experiments to find empirical data about gene function…

An ERV insertion found at the same spot in the same gene in two different species would be an orthologous ERV. Orthology has nothing to do with function. It has to do with position in the genome.

All that means is that there was positive selection for mutations in those ERVs which caused them to diverge at a higher rate than predicted by neutral drift.

Humans don’t have PtERV insertions, so I’m not quite sure where you are getting that from.

Non-functional DNA can also be orthologous. Orthologous simply means being in the same position in each genome. It has nothing to do with function.

That’s because ENCODE uses a definition of function that simply means “it does something”. This is not the definition that other scientists are using. If a stretch of DNA is transcribed into RNA at least once in one cell, then ENCODE considers it to be function even if that RNA has no impact on the fitness of the organism. The vast majority of biologists define functional DNA as DNA sequence which has an impact on fitness and will therefore show some evidence of sequence conservation. ENCODE includes junk DNA in their definition of functional DNA because even junk DNA will be transcribed into RNA at low levels.

About 2-3% of the human genome is made up of genes.

You falsely assume that there is only one right sequence of DNA.


Here are some references from an old BL thread discussing the ENCODE project:


Obviously such will not have An Upper Limit on the Functional Fraction of the Human Genome from 2017 or On causal roles and selected effects: our genome is mostly junk also from 2017 that is a review type of paper on the topic.

I’m not sure how exactly your yeast paper has anything to do with all the papers written on human beings where much less than 20% has any function in the sense of fitness.

But they have not been heading this way… for a whole decade. The only paper at all was the ENCODE project which is discussed in length above… certainly they had a very “liberal” definition of function that many non-experts jumped on.

Also function has nothing to do with the ERV evidence.


Not in the sense that any other study (or human being, really) uses the word ‘function’. The comparable number from ENCODE is around 11%.

That’s 90% of genes (protein-coding genes, specifically). I would expect at least 90% of human genes to have functions, too. But protein-coding genes make up less than 2% of the human genome.


Any activity involving creating phylogenetic trees involves a few basic assumptions. Whether its morphology, or computations of genetic similarity, the following assumptions are basic.

Three things assumed are -

  1. Change in characteristics occurs in lineages over time.
  2. Any group of organisms is related by descent from a common ancestor.
  3. There is a bifurcating, or branching, pattern of lineage-splitting.

This is a misunderstanding on your part. For example, if you make phylogenetic trees from genes associated with echolocation between Bats and Dolphins, you would get some thing like this :slight_smile:

As to phylogenetic signals. It involves removing genetic noise (genetic information that does not tell us anything about lineage) and thus is a filtered result in itself.

Anyway, with respect to your comment on jelly fish and mice… would Squids and human beings do?
As is well known, Squids and human beings have eyes of the same type. Recent studies have shown that the development of the camera eye in Humans and squids happen through the same gene called ipax6. The differences in ipax gene for squid which allow the squid to develop camera eyes are not shared with other molluscs and so this is assumed to have evolved “convergently”.

In summary, we identified the acquisition of splicing variations of Pax-6 in cephalopod eyes (Figure 4) and found that the acquisition occurred independently in vertebrates and cephalopods. These Pax-6 splicing variations in cephalopods were controlled spatio-temporally during eye formation. Although the acquisition of camera eyes in the cephalopods is yet a problem, Pax-6 variants in cephalopods have been acquired in a lineage-specific manner.

Of course, now evolutionary biologists are speculating that a common ancestor (of the octopus and humans) had these genes and they were lost. I am going to quote from an article below which argues for “constrained genes” in octopus-

In spite of the evolutionary divergence between octopuses and humans, 69.3% of the genes examined (729 of the 1052 genes) were commonly expressed in the camera eyes of human and octopus. Moreover, comparison of octopus-eye ESTs with genes in the human connective tissue indicates that the similarity of gene expression between human and octopus eyes should be remarkable. Note that the increase of gene expression similarities
between human and octopus eyes from 15% (162/1052) to 69.3% (729/1052) is caused by the increase of the EST data set of human eye from only 3809 ESTs in the database of BodyMap to 13,303 human-eye ESTs in the combined database of NEIbank, MGC, and BodyMap. This observation suggests that many more similarities of gene expression between human and octopus eyes will be observed when the EST data increase further.
Although these 729 genes might contain housekeeping genes because the 44 genes were also found in the ESTs of human connective tissues in BodyMap, we found that many more
genes (118 genes) were specific to the camera eye in this case. Therefore, we suggest that these 729 genes contain genes necessary for the developmental process and biological function of the camera eye.
For the evolutionary origin of the gene set working for the camera eye, we observed that 1019 genes existed in the genome of the common ancestor of the bilaterian animals. Although the morphology of the ancestral eye cannot be inferred from this study,
we were able to provide strong support for the hypothesis that these genes having had an important role in the function of camera eyes in both humans and octopuses were present in the last common ancestor of these two lineages.

We found that some of
the genes conserved between humans and octopuses have been lost in the organisms having no camera eye structures.This result supports a hypothesis that the genes required for the development and maintenance of the camera eye were retained in the vertebrate and octopus lineages, but lost in insects,nematodes, and tunicates. For insects, it is likely that the
genes having functions specific to the camera eye were not important for the evolution of the compound eye, and therefore must have been lost from the genome.
So the answer to your Jelly Fish, mouse claim is simple. There are three possible evolutionary scenarios -

  1. They both gained similar genes through parallel evolution/convergent evolution.
  2. There was a common ancestor with these genes. These genes were conserved in the two lineages and lost in everything else (what a relief there are no actual common ancestors of intermediate species to actually verify all this!)
  3. Any combination of 1 and 2 which either works or leaves people so confused, they dont know which is which.

Well, first of all we do not see such a clear relationship between similarity and common descent.
refer discussion on development of the eye given above.

There are different ways to define function.

Despite the pressing need to identify and characterize all functional elements in the human genome, it is important to recognize that there is no universal definition of what constitutes function, nor is there agreement on what sets the boundaries of an element. Both scientists and nonscientists have an intuitive definition of function, but each scientific discipline relies primarily on different lines of evidence indicative of function. Geneticists, evolutionary biologists, and molecular biologists apply distinct approaches, evaluating different and complementary lines of evidence. The genetic approach evaluates the phenotypic consequences of perturbations, the evolutionary approach quantifies selective constraint, and the biochemical approach measures evidence of molecular activity. All three approaches can be highly informative of the biological relevance of a genomic segment and groups of elements identified by each approach are often quantitatively enriched for each other. However, the methods vary considerably with respect to the specific elements they predict and the extent of the human genome annotated by each

The evolutionary view of function as something on which selection acts upon is a tautology.I dont see it as either valid or particularly valuable.

Anyway, the important thing is that the NIH which funded ENCODE is looking at it from a prevention/cure of disease point of view and so they should do a more thorough empirical search than any evolutionary biologist.
Hence my optimism.

Its an example of empirical studies vastly increasing our knowledge of function in genes.
There are similar studied in progress on the human genome also which should push the envelope on “function”

Perhaps… i am not sure though. The paper keeps claiming that their study is “genome wide”… (I have given the link for the paper,you can verify it yourself).
Also recently, John Hopkins started a project to create a synthetic yeast cell. They claim the yeast cell is 8% smaller than the natural yeast cell after removing “junk DNA”

One exciting feature of the synthetic genome is that it’s about 8 percent smaller than the natural yeast gnome. Genetic sequences that can make DNA disposed to mutations and instability were relocated and noncoding “junk” DNA was removed.
So these guys obviously felt some need to keep 92% of the genome.

However, i just pointed to the paper as a example of how concerted empirical/laboratory work can vastly increase the percentage of the genome with known functions.


I bet you didn’t even realize how you mangled the science on Squid camera eye and human camera eye.

Humans and squid evolved same eyes using same genes

The gene cited has a common ancestor… but that gene’s sequence for humans is NOT the same as the sequence for that gene used in Squid!

In fact, it suggests that there was a common population for use of the original version of master controller gene… and that the squid version sent squid eye in a direction different from how fish and human eyes developed.

In other words… the master eye gene Diverged!

Help him, @T_aquaticus, if you have the time.

Can you cite any paper that shows how different the gene is?
Having a common ancestor means the genes show homology… I.e they are similar.
I suggest you read the second paper I cited, or at least the part I quoted.

I don’t know where you got this from. Even the article you linked to doesn’t say anything of the sort.

Let me repasts the quote from the paper I cited.

I couldn’t find any document saying pax6 genes of humans are more similar tot hat of fish as opposed to cephalopods… is that what you are claiming? Can you share your source for the info?

@Ashwin_s (@pevaquark & @T_aquaticus )

The reason you don’t recognize the signs that genetics are diverging is because you
only notice the similarities being described, rather than the differences that emerge in
an “ancestral” control gene, in order to make what you think are “the same” eye.

Yes, both eyes are “camera box”, but that’s just one level of the nested hierarchy.
Labels in nested hierarchies are not arbitrary or tautological, because the labels are
based on Actual Differences in the biological structure. You are right that human language
can be rather arbitrary - - but you incorrectly attempt to make the arbitrariness of language,
and of the humanly subjective selections made by an investigator, as equally arbitrary.
If there are REAL differences, then the point of the nested hierarchy is to track the changes,
where they might have come from, and the pattern of where a change has ended up.

[[ Be sure to click on the image to maximize font size! ]]

[[ Be sure to click on the image to maximize font size! ]]

Computational phylogenetics tests those assumptions. If those assumptions were not correct then you wouldn’t get a phylogenetic signal.

When you compare the whole Prestin gene you get the expected phylogeny:

“Repeated analyses of phylogenetic reconstruction based on nucleotides corresponding to variable amino acid sites only (414 bp), thus reflecting areas of nonsynonymous change, also recovered the putative gene tree topology with strong support for the clade of laryngeal echolocators (62% ML bootstrap and 97% BPP). Conversely, analyses of the remaining nucleotides (1,800 bp) recovered the species tree, albeit with reduced support for the Yinpterochiroptera clade (<50% ML bootstrap, 47% BPP). Therefore, the monophyly of laryngeal echolocators is supported when only those parts of the gene that lead to amino acid changes are analyzed, but this arrangement is lost and laryngeal echolocators become paraphyletic (as suggested by recent molecular phylogenies) when areas of the gene that do not result in amino acid changes are analyzed.”

What gene do humans have that is an exact copy of a jellyfish gene that is also not found in any other vertebrate? That was the challenge. All other vertebrates have Pax6, and the sequences produce the expected phylogeny.

You can check out mouse Pax6 here:;g=ENSMUSG00000027168;r=2:105668900-105697364

Zebrafish Pax6 here:;g=ENSDARG00000103379;r=25:15029041-15049781

As to the structure of the eyes themselves, the cephalopod and vertebrate eyes are very different. The retinas in each develop from different cell types and the retinas face in opposite directions.

They are found in numerous vertebrate species which fails the challenge that was given.