We have been gibbering for many, many pages, at least nominally on the topic ‘Common Design vs Common Descent’. I’d like here to discuss an interesting fact I discovered during the course of this. I mentioned it twice, but readers seemed underwhelmed by what, to me, looks like a genuine scientific discovery (I haven’t searched exhaustively for priority). More importantly for present purposes, it provides a useful test-bed for several concepts that regularly do the rounds.
Sal Cordova had latterly been pursuing an attempt to demonstrate using freely available phylogenetic tools that tetrapods are not descended from aquatic, gilled vertebrates – what we conventionally call ‘fish’. In the process, Sal chose to use gene sequences of what turned out to be cytochrome oxidase (COX) – a component of the electron transport chain in mitochondria and in prokaryote plasma membranes. This molecule is ultimately what that breathing thing is all about – the molecular oxygen we inhale, in diatomic clumps, is held together by electrons shared between the atoms; COX donates electrons passed along from cytochrome c which enable the oxygen atoms to be separated; these react with protons (a different reaction for each of the two atoms) to form water. In the process, additional protons move across the membrane to generate an energetic imbalance that can be tapped, much like a pumped-storage hydro-electric scheme, to make ATP.
Sal thought he was looking at cytochrome c – this molecule is actually one step ‘upstream’ from COX, supplying it with the electrons which the latter passes on to oxygen. In eukaryotes, it so happens that the cytochrome c gene is in nuclear DNA, while COX is in mitochondrial DNA. This creates a significantly different evolutionary environment for the two genes, due to the proximity to reactive molecular species in the latter and the different dynamics resulting from recombination in the former. It would be unwise to draw too many evolutionary conclusions without an awareness of this distinction.
During the course of this discussion, Rumraket took some sequences of the actual cytochrome c, the molecule Sal thought he was looking at, and ran a Uniprot process to generate a phylogeny for a set of sequences. In an idle moment, I thought it might be interesting to explore the taxonomic neighbourhood a bit. It seems to me fundamentally inconsistent to dismiss phylogenetic inference on the grand scale while accepting it more locally. Of course it’s not clear whether any Creationists accept it locally either! I’ve tried repeatedly to get someone to say at what taxonomic level they think Common Descent stops being a valid inference; no luck so far.
So here’s what I did. I was interested to see what the cytochrome c’s of close relatives of the salmon looked like, rather than the grand-scheme analysis being pursued by the ‘I-ain’t-no-fish’ brigade. So I took Rumraket’s sequence for the Atlantic Salmon Salmo salar. The BLAST came up with several paralogs – gene duplicates – in the salmon, and orthologs – genes in separate species – with >90% sequence identity. I say this a lot, but the only process I am aware of that leads to sequence identities in anything like that ballpark is nucleic acid polymerisation. This mostly happens during cell replication (DNA-DNA) and gene transcription (DNA-RNA), somewhat less often by reverse transcription from RNA to DNA. So, absent another process that generates such extensive identity, common descent (at sequence level) has to be a front runner for the reason for any such highly alignable sequences.
So, here are the top few hits for Salmon cytochrome c sequence B5XFR7 (link here but be quick; I don’t think these are archived for long):
Rainbow Trout (Onchorhynchus mykiss) C1BFD3 99%
Salmon paralog B5DFW1 99%
Salmon paralog B9EMZ7 98.1%
Rainbow Trout paralog C1BGL1 98.1%
Rainbow Trout paralog C1BG90 95.2%
Salmon paralog B9EMJ0 94.2%
Rainbow Trout paralog C1BFB8 94.2%
Large Yellow Croaker (Larimichtys crocea) 94.2%
Sea louse (Caligus rogercresseyi) C1BPA2 93.3%
Rainbow smelt (Osmerus mordax) C1BKE6 93.3%
… ?
Whoa, back up a bit … the sea louse? That’s a crustacean. Now, I look up this organism and, it turns out, this is a parasite of both Rainbow Trout and Atlantic Salmon, particularly in Chile (yes, they farm Atlantic salmon in the Pacific). So, pending more work, a viable explanation for the high sequence identity with Salmon and Rainbow Trout is gene transfer from one or the other (hard to tell which). If not HGT, it was a remarkable coincidence that the words ‘salmon’ and ‘trout’ should leap off the page when I looked up the organism.
A naive user of free phylogenetic software might try and argue that this anomaly completely destroys the use of such software. After all, a phylogeny based only on cytochrome c might perch this crustacean slap dab in plaice in the middle of the Salmonids (it could also be used to show that salmon are more closely related to trout than they are to their own genes, in clumsy hands …). This is obviously a bit fishy, because we know (ask yourself: how do we know?) that it doesn’t belong there.
So, here are a few questions for Creationists to consider.
1) Do you accept that high sequence identity is reasonably inferred to indicate an origin in a single ancestral DNA sequence?
2) If so, do you agree that the paralogs – multiple copies in the same species – likely share common ancestry with an original single sequence?
3) How about within the family Salmonidae, to which both Atlantic Salmon and Rainbow trout belong (the trout is actually in the same genus as the various Pacific salmon)? Do you think sequence commonality highly likely indicates a genetic relationship here too?
4) Do you agree that the likeliest cause of high sequence identity in the sea louse version is due to gene transfer from salmon or trout, given its intimate association with these species?
5) What makes us think that the sequence in sea lice is anomalous, rather than indicating an actual whole-genome pattern, without even looking at the genome?
6) For broader genomic comparisons, collecting together multiple gene trees, where in the standard taxonomy would you place the division between the region that is reasonably inferred to result from common descent, and that which is not?
Another issue relates to function, and the need or otherwise for functional variation among species or among paralogs. As discussed, the task of cytochrome c and COX is chemically quite low-level – to pass electrons on down a chain. On a design paradigm, the fact that this function needs to vary at all is rather curious, unless we allow that variation can occur through largely neutral mutation. Even stranger is the fact that variation within a single species among its various paralogs is of the order of that between some orthologs in separate genera of the Salmonidae. If one answered ‘yes’ to 2 but ‘no’ to 3, one is saying that the same amount of sequence identity is diagnostic of sequence relationship + mutation in one case, but not the other. One might appeal to evolutionary unnattainability of a transition, but it doesn’t seem to me that the gap between salmon and trout is unbridgeable, starting from a common ancestor. After all, as noted, Pacific ‘salmon’ are more closely related to trout than they are to Atlantic Salmon (I’m curious no other Onchorhynchus species came up, but this may be due to lack of sequences). So, it seems plausible to me that all these gene variants are commonly descended, through fully connected paths of nucleic acid polymerisation.
This pattern of otherwise inexplicable variation of non-morphological genes is repeated throughout the genome and throughout nature. ‘Common-Designists’ would have it that there’s a Psilocybe way of dehydrogenating lactate, and a yeast way, and a bottlenosed dolphin way. And there’s a dandelion way of passing electrons on, and a squirrel way, and an E coli way, and a sea louse way … but hang on; the sea louse way is pretty close to the salmon way, in this gene copy at least. If this is an HGT event, it indicates that there is much less species-specificity in function than some would argue. If HGT, this is a natural experiment, placing a variant in a distant relative and seeing how it fares. Assuming it’s not a pseudogene, the sea louse is apparently able to use the cytochrome c of a very distant relative in addition to its existing repertoire, with no obvious adverse consequences. More work would establish which of its isoforms tend to be preferred, but nonetheless the bare fact rather goes against the expectation that these proteins are highly clade-specific for design reasons. And indeed it does seem much more likely that low-level function can be passed around without excessive penalty than more taxon-specific genes – the variants are mutational fluff, not critically functional. This is one reason why Amino-acyl synthetase phylogenies are actually quite poor – extensive HGT is possible, because really, how many different ways do you need to stick an amino acid on the ACC- end of a tRNA?
TomMueller,
Cheers Tom!
Allan Miller,
On what basis do you make this claim? Cytochrome c is either active during embryo development or it is not. The lack of a forehead is evidence it is and is critical to embryo development. You made a baseless claim and you are denying conflicting evidence based on the not necessarily argument, Why would you claim that it is trivial that some mutations cause dramatic effects in development? Your claim of this being trivial is an argument from ignorance.
No, we just need to discover that some are.
Unfortunately my good man this is the way you have set the game up 🙂
Plenty of divergence if there was created heterozygosity and/or accelerated mutation.
No.
Regarding Eukarytic gene transfer, I know two YEC colleagues who were genetic engineers, the famous one of course is John Sanford the other is Rob Carter who was a pioneer of glowing fish.
I asked how they did it. Fundamentally, the DNA from one creature has to puncture the cell and probably reach the nucleus. Rob used electricity and pipettes to inject eukaryotic DNA. John Sanford put DNA on a golden bullet and shot it into the cell. The ones that didn’t die sometimes incorporated the foreign DNA. Will this work for essential genes like aaRS or Topoisomerase? I don’t know for Eukaryotes.
I don’t recall the story with Rob Carter exactly, but he told me he was gathering genes from cnidarian species on the sea shore that glowed. He manage to inject that DNA into fish to make them glow. He used pippetes and electricity.
Please don’t quote me as saying my account was definitive, but that’s the best of my recollection. He’s he one to ask, or we could look to other examples of Rob’s competitors who were successful making glowing fish.
The paper I have related to some of his work:
http://scholarlyrepository.miami.edu/dissertations/2003/
Yes, because wiki is a creationist censoring enterprise. But I linked to the paradox because there are secular researchers who are still working to solve the paradox. The fundamental problem is the sun’s intensity is changing over time. There has to be some sort of thermostat that keeps temperature stable. Thermostats are usually designed.
If the paradox is solved by (gasp) green house gas global warming, how is the environment miraculously undoing the green house gases in a manner that is just right for every change in the sun? If you believe in climate change and all the dire warnings, you should be the first to wonder how the earth managed to be in the goldilox zone of not too much, not to little green house gases.
As for the other factors you mentioned, they have to be fine tuned to put Earth in that Goldilox zone.
This is by Danny Faulkner, professor emeritus of astronomy, University South Carolina. He now works for AiG.
http://www.icr.org/article/young-faint-sun-paradox-age-solar-system/
So what you mean is that if you are allowed to invoke vast numbers of miracles you can accommodate any amount of divergence. But in that case you can place no limit on divergence, so what’s the point?
Isn’t that a very serious problem for you?
Is it the only medium?
Wiki’s policy is to remove obvious disinformation and outright lies. Unfortunately most everything Creationists post to Wiki regarding science falls into those categories.
Adapa,
Who decides what is disinformation and lies? Jimmy Wales?
You have a point. We mere mortals have no reliable hotline to Absolute Truth, and must fall back on such imperfect substitutes as observation, evidence, logic, and consistency. And while I doubt anyone would regard these as perfect, deploying them for the last few centuries has dramatically changed our lifestyles in ways most people appreciate. Bottom line: these things WORK, often enough to consider them useful and even important.
Flint,
The proposition has been made that Wikipedia is biased against certain viewpoints, namely creationism, or anything that is anti-evolution. So just saying we rely on observation and logic is meaningless. Whose observation, whose logic?
I believe the “evidence” as you call it is quite clear, Wikipedia intentionally slants all its content to fit the agenda of its founder Jimmy Wales- an outspoken atheist, propagandist.
Sal et al. should take their Young Earth discussion to another thread or start a new one. This one was about sea lice and salmon and a claim of HGT.
colewd,
You can mutate many genes and generate developmental abnormalities without that proving that the genes in their unmutated form are critical for the thing the mutated form affects.
It’s trivial because it does not impact upon the issue. The ignorance is largely yours; you don’t appear to have a clue about the relationship between mutational consequence and the ‘native’ isoform. If I mutate a gene and that has a consequence, it does not mean that the unmutated form is vitally involved in the pathway in which the consequence is manifest.
And, there is a difference between the incidental apoptosis of cell damage and the apoptosis of development. We have 3 or more DNA repair pathways for example; why would we just have one apoptosis pathway? You have done no work to show that the cytochrome c isoform is critical for the final form of the organism, merely waved an arm in the direction of a couple of facts as if proof. And if that doesn’t work, utter the lamest of ‘well, we don’t know everything’ excuses.
And once again, you are obsessed about animals. In fact, probably obsessed just about chimps and humans. Although the thread is about a couple of animals, the principles of evolution go way beyond our clade. If cytochrome c’s criticality for development is an issue, we need simply pick another molecule, or another clade. Unless all DNA sequences are critical for the morphology of an organism, you are simply obfuscating by obsessing over one piece of wood, pretending there is no forest.
We already know some are. I fail to see why finding ‘some’ would tell us about why they all have this approximate congruence with the morphological tree.
You’ve lost me.
Hi Allan. Don’t worry. I didn’t miss your discovery, but didn’t have time to take a look into it. My first thought was also that it might be a contamination.
So where did the sequence come from? Was it a whole genome sequencing effort? Was there a de novo alignment? On what contig was your gene placed?
I was going to check those things myself, but maybe you already covered that.
stcordova,
That’s actually the whole point. I am inclined to give a qualified ‘yes’. Unfortunately, it’s not slam-dunk for-sure possible because the rest of the molecular repertoire evolves in the presence of the given isoform, and may be impacted negatively, but as far as the isoform itself is concerned, there seems no compelling reason for the variation we encounter in these ‘low-level’ proteins, and one could indeed substitute for another. Opening again the question of why the variation would follow the morphological tree.
To repeat my mantra with a slight variation, there does not need to be an amoeba way of topoisomerising, and a duck way, and a stinkhorn way …
There have been numerous experiments where a long-distance transfer has been genetically engineered. I recall one (can’t find it at the mo) in which a mouse knockout was ‘rescued’ by a gene from a fungus. It did not grow hyphae; it was just a mouse.
Whether this is HGT or not is important, but I have a point to make either way. We can use ‘forensic’ techniques to find out a bit more about it. If it’s contamination, as it may well be, we can establish that by getting another sea louse, from a known host, being a bit more careful, and seeing if it too has this gene. If it doesn’t, we can tentatively conclude ‘contamination’, and people of all metaphysical persuasions are happy to accept the fundamental point that this sequence is commonly descended – commonly descended with a gene in other salmon.
If it does have the gene, we can find out where it is in the sea louse genome, and see how much of the flanking sequence is more closely related to the salmon. But what are we doing now? We are assuming that the sequence is commonly descended with a gene in the salmon, otherwise why on earth would there be flanking sequence as well? OK, suppose we don’t find that, but we still have the ‘salmon’ gene sitting there in the sea louse genome. How did it get there? It could still be commonly descended with a salmon gene. If it happened in the last 6000 years, we’re fine, it’s allowed to be commonly descended with a salmon gene! So we can cast our net wider; go for greater coverage of both sea lice and salmonids, and see what the pattern is. On common descent, we’d expect a pattern. On ‘common design’, we wouldn’t.
Either way, it is still a curious little feature, for people so sure that the same sequence must have a different cause depending on whence it came and how recently. How do we even know it’s anomalous? Because we expect sea louse genes to be more different from salmon genes than that. Why?
As has been explained to you many times before, nobody claims that a designer cannot design congruent nesting hiearchies. But as has also been explained to you, there’d be no reason for the designer to do that. It is not a valid strategy. It can serve only one purpose: You want to make it look like there was common descent.
It doesn’t make the designing process any more clever, or efficient, or whatever you could imagine as a reason for it. This is why it doesn’t make sense to claim that a designer “did it on purpose”. Yes, a designer COULD do it like that, but why WOULD a designer do it like that? What purpose does it serve? It has only one effect: It makes it look like there was common descent.
Do you understand this, Bill?
Corneel,
I’ll be honest; my due diligence was pretty slack! This being TSZ, enormous effort can bring scant reward 😉
I just slapped one of the salmon sequences (actually, not even the whole thing) into BLAST. The original query was here and a second query, checking for possible 100% sequence identity starting with the sea louse sequence, was here.
I think wikipedia is actually not so “biased against creationism and anti-evolution”, as it is just generally pro-science biased. As an encyclopedia should be.
If you go and edit the physics articles to show how the Earth is flat, or the center of the universe, you will also discover that this will be “censored” away.
And the same thing for homeopathic remedies and other purported miracle-cures, the healing powers of crystals, that vaccines and condoms don’t work, or that only gay people can contract HIV etc. etc.
Or that Adolf Hitler and Barack Obama are secretly alien lizard-people who control the world with black helicopters, chemtrail and “fema camps”. That the pyramids are landing pads for UFOs. Or that the holocaust didn’t happen, or countless other fringe crackpot views.
It might not be perfect, but an encyclopedia should not present any and all fringe crackpot views as if they have equal merits or support within the scientific (or historical) community. It should simply present what is the established science and history at the time.
I found another sea louse cytochrome c on uniprot. Turns out there are three different cytochome c’s listed for sea lice.
The species you found has to different ones listed:
>|C1BN51|C1BN51_CALRO Cytochrome c OS=Caligus rogercresseyiGN=CYC PE=2 SV=1
MGDIKKGKSLFVKKCGQCHTVEAGGKHKVGPNLHGLIGRKTGQAPGYNYTAANIGKGITWSDETLDE
YLINPKKYIPGTKMVFAGLKKAGERKDIIAYLIDSTK
and
>|C1BPA2|C1BPA2_CALRO Cytochrome c OS=Caligus rogercresseyi GN=CYC PE=2 SV=1
MGDIAKGKKAFVQKCAQCHTVENGGKHKVGPNLWGLFGRKTGQAEGYSYTDANKSKGIIWETDTLM
TYLENPKKYIPGTKMIFAGIKKKGERVDLIAYLKSATS
There’s another species of sea lice, with a cytochrome c:
>|C1C347|C1C347_CALCM Cytochrome c OS=Caligus clemensi GN=CYC PE=2 SV=1
MGDIAKGKSLFVKKCGQCHTVEAGGKHKVGPNLHGLIGRKTGQAPGYNYTDANISKGITWSPETL
DEYLINPKKYIPGTKMVFAGLKKAKERNDIIAYLVDSTK
This is the alignment: Bigger picture.
I think the one you found, which is very close to the salmon one, is a contaminant, as the sea louse Caligus rogercresseyi has two listed cytochrome c’s, and one of them is much closer to another sea louse Caligus clemensi cytochrome c.
Here’s one with salmon included. bigger pic.
Interestingly there is still a single amino acid substitution separating Salmon salma cytochrome c, and the Caligus rogercresseyi cytochrome c-entry C1BPA2_CALRO.
Rumraket,
It may well be a contaminant, but that doesn’t follow necessarily from the pattern you mention. Naturally, the sea louse would have more ‘crustacean’ versions of the gene, prior to any putative transfer, and hence after.
Rumraket,
Yes, that’s what persuades me not to wholly abandon my HGT notion, although sequencing error or contamination from a non-annotated source are clear possibilities.
OK, here is the source:
http://www.uniprot.org/uniprot/C1BPA2.txt?version=25
RP NUCLEOTIDE SEQUENCE.
RC TISSUE=Whole tissue {ECO:0000313|EMBL:ACO10855.1};
RA Yasuike M., von Schalburg K., Cooper G., Leong J., Jones S.R.M.,
RA Koop B.F.;
RT “Caligus rogercresseyi ESTs and full-length cDNAs.”
Yasuike published some papers on these sequences so I will check out what they have done. At a glance, it looks like they extracted RNA from whole organisms and built an EST library out of that.
The Sea louse sequence C1BPA2_CALRO is unreviewed, with a score of just 2/5, so caution is obviously merited. Nonetheless, numerous articles indicate parasite-host interactions as a rich source of eukaryotic HGT events. Unfortunately, also an obvious source of cross-contamination, as one would obviously need to avoid sequencing the parasite’s lunch!
Expressed Sequence Tags give no information about flanking sequence, which makes it difficult to rule out a contamination, I am afraid.
The sea lice looked awfully familiar, and then I realised they resemble Cyclops copepods that I dicovered as a kid looking trough my microscope at pond water.
Corneel,
Well, the flanking sequence wouldn’t rule out contamination either I guess. I was thinking more of actually locating the gene in the genome once one had definitively established its presence, and then working outwards.
[eta – though I guess EST does point to it not being an unprocessed pseudogene, so rules one thing out]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280385/
It does perturb me that they talk of ‘whole-body’ extracts. Surely you wouldn’t just put the animal in a blender? Isn’t that asking for trouble, in any species?
Compare nucleotide sequence for salmon and C rogercresseyi cytochrome c’s. If there are lots of silent substitutions separating them, that could indicate HGT?
Rumraket,
I was just hunting for the DNA sequence (although again, contamination from a non-annotated genome would be possible).
That’s what I meant. But if they only sequenced cDNA from expressed sequences, all positional information is lost. I am not even sure there exists a whole genome sequence for this species.
Corneel,
Yes, you’d definitely have to go back to the organisms. But, as I mentioned in an eta above, we can rule out ‘unprocessed pseudogene’ at least.
I agree, so therefore Allan shouldn’t be putting my name in the OP and posing questions specifically to the creationists at TSZ knowing I might give answers from a creationist perspective and provide arguments for my position.
So I will defer to Joe’s request out of respect for Joe. Goodbye from this thread.
stcordova,
Your name was mentioned as part of the background to this topic. I felt it useful to abstract this question on detailed, local sequence comparisons from the bloated mishmash the ‘Common Design/Common Descent’ thread has become, as I felt this (to me) interesting coupling of issues had become buried. Since it was inspired by and directly related to that thread and the questions within it (including cautions on reliance on simplistic BLASTs), I make no apology for the construction of this OP.
Alllan,
Nor should you. Sal’s complaint is off-base.
How about a naive user of non-free phylogenetic software?
ETA: Or taxpayer funded phylogenetic software?
Rumraket,
Why would the re use of parts not show a pattern like this? In the case of cars new designs do not abandon older parts where those parts still do the job.
Allan Miller,
Science does not prove anything. Can you show an example where you mutate a gene a developmental abnormality occurs and it is demonstrated to not be part of the developmental process?
Example please.
I have provided an experimental example of a single nucleotide change to cytochrome c and a mouse forehead not forming. You have not provided an alternative explanation of why this event could happen with cytochrome c not being involved in development. This is exactly the type of experiment that tells us how a cell functions.
We know the forehead is fine with a standard cc sequence. We modify the sequence and the forehead does not develop. Looks to me like the protein was involved.
colewd,
Jesus Christ, Bill.
Theobald’s 29+ Evidences addresses this exact issue.
You didn’t actually read it, did you?
Do they refuse to use new parts and systems that can’t be built out of the older parts?
IOW, are autos ridiculously derived from ancient parts like life is?
And have you ever actually thought about any of this, instead of objecting to everything that goes against your beliefs?
Glen Davidson
keiths,
Sure I did, and it is a vacuous argument. Do want to make an argument or are you just going to have someone make it for you. Show how the pattern we see is not just the result of the logical re used parts in a design process. Show that the level of divergence is not best explained by design.
It’s pretty simple, although you manage to miss it constantly.
Bird and mammal genomes “share knowledge” only prior to divergence, hence the homologies are old. After divergence there are no longer homologies. Therefore bird wings and bat wings share tetrapod homologies, but lack any homologies in adaptations for flight.
Autos and planes share the “new homologies.” Thus jet engines–which are not derived from piston engines–spread across Boeing, McDonnell Douglas, Lockheed, Russian manufacturers, British firms, etc. Why don’t bat wings share feathers–which are wonderful for shaping airfoils–with bird wings?
How do you manage to avoid this colossal difference from manufactured goods, no matter how many times it’s pointed out to you?
Glen Davidson
BiIl,
You clearly don’t understand Theobald’s argument.
Quote the part where you think he goes wrong, and explain why. We’ll try to straighten you out, though I don’t hold out a lot of hope.
keiths,
I think you have demonstrated solidly that you do not understand this argument by your failure to make your own case.
Quoting a source should support argument not assertion. I think Theobald is deeply flawed because it is 13 years old and a lot of new information about molecular biology has surfaced since then. He also assumes that the alternative to his hypothesis is also random so his arguments do not counter the design argument.
I want your arguments not Theobalds. I am not interested in a 13 year old paper at this point that does not defend his arguments against design.
Hi Allan
I would be grateful if you could provide references
ITMT
check out
http://sandwalk.blogspot.ca/2017/11/lateral-gene-transfer-in-eukaryotes.html?m=1
colewd,
I’m not sure what you think the ‘developmental process’ is. Is normal mitochondrial function part of it? It is essential for all organisms, at all stages of their life – mutate it and you get ‘developmental abnormalities’, or even nothing, but it does not appear to directly control the form of the organism that develops in unmutated form. That is largely down to molecules that affect gene expression, not proteins like Cyt c.
No, I’m not dancing to refute a preposterous case. One developmental abnormality from a specific mutation, of the many millions of mutations that can occur, does not even address the case that the cytochrome c variation we see is non-neutral and intimately linked with the form of the organism. Especially since organisms as different as human, chimp, orang utan, gorilla, and several species of gibbon all share the exact same isoform, to take just one example of the kind of clade variation you have to account for with no actual variants.
That fact alone makes me wonder why I am bothering pandering to this futile pursuit. Add to this the fact that the paralogs in the salmon – the cytochrome c’s in a single fish – differ by about as much as the difference between any two primates.
Look elsewhere for the ‘morphological code’.
TomMueller,
Hi Tom,
Yes, I saw the Sandwalk piece, and discussion; interesting.
I didn’t originally post because I couldn’t find full text or everything, but try:
http://www.sciencedirect.com/science/article/pii/S1471492213000731 (paywall)
http://www.pnas.org/content/113/45/E7010.full (full text)
https://www.ncbi.nlm.nih.gov/pubmed/19271205 (paywall)
Allan Miller,
Allan Miller,
This is the process that takes you from an egg to a fish.
This is statement you continue to make despite the evidence. You are confirming that evolutionary indoctrination is a destructive filter in understanding advances in biology.
The only conclusion I can make here is that all you have is an assertion based on the evolutionary paradigm.
Your conclusion from this is?
Where would you suggest he look?