I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.
Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.
If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.
One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.
Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.
That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).
Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.
The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”
So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.
So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.
And once again you ignore most of the comment in which the little bit you do respond to is contained. I hope you will consider that also to be a fair and accurate criticism.
Because some sub-species that look so different turn out to be strong candidates for a common ancestor after hybridization experiments are conducted.
From the YLC (Young Life Creation) standpoint — say life younger than a few million years, maybe even 6,000 years, there is only so much mutation that is believable to allow sufficient change. For example, I don’t think a few million years would be enough time to evolve a rat into a monkey, or an amphibian into a bird. So there are baramin based on the orphan features. The large groups of Baramin seem identifiable, but baramins with small differences are not as easy to identify.
Hybridization experiments convince me the following are members of a created kind. The definable “clades” within the baramin would be lion and tiger:
I was an evolutionist, I don’t think the physical evidence convincingly shows the fossil record is old, it looks young to me, hence I have identified myself as a YLC long before identifying also as a YEC. If the fossil record is young, then that counts as strong evidence of Baramin (the Orchard Model) vs. the Universal Tree of Life. As I said in the OP evidence in favor of a young fossil record (YFR) is evidence in favor of common design as the explanation of the nested taxnomic hierarchies.
No I’m saying that while questions of the one true tree are interesting, they are besides the point. Which is this:
1. One can infer common descent to a virtually total certainty.
2. Without being able to determine the exact branching pattern of the diversity of life.
There is no logical conflict between those two statements. Your Elliot Sober quote is, by you, apparently deliberately brought up because you want to make it seem like there is a problem with 1. But the quote pertains statement 2.
I guess, rather than dishonesty, you might just be so ignorant you don’t actually understand the remit of the Sober quote. I have to concede that is entirely plausible.
Face up to them you say to me? I’m the one that took the time to actually explain in my own words the remits of Elliot Sober’s words.
Why don’t you face up to the facts I detailed?
Actually we do know which one is best, and we know why it is best, but we also know that there are problems associated with applying the best method (maximum likelihood or bayesian methods), for example that you need a substitution model, and there can be serious doubts about what substitution model to use because differences in the rates and distribution of substitutions (like transversions versus transitions) vary over time and between lineages.
See, again I’m both facing up to the facts, and explaining what they are in my own words, for the purpose of clarification.
You’re not here to offer clarification and increase understanding, you are here to obscure and propagandize.
Rich, coming from a guy who affirms common descent.
It’s a big if, Sal. You have to reject so much reality and for what? The Old Testament is irrelevant to Christianity. That starts with Christ. I guess that is why they call it the New Testament.
There’s a great article by Jonathan Kane at The Panda’s Thumb that might be written for you.
And that marks the only attempt in this long post to answer my question, which if I may remind you is “Why can’t we easily identify baramins?”. And not even the above is an answer. Are you incapable of a direct response? (If you think that was a response, please explain.)
Here are some questions. I have separated them to make it more convenient for you not to ignore them.
What evidence is there that life is significantly younger than the earth (say, less than half)?
What evidence is there that life is less than billions of years old?
If there is no tree of life, why is there a nested hierarchy?
If life is young, why is there a faunal (biotal) succession?
If life is young, isn’t that a greater reason to expect that baramins should be easily distinguished?
Why can’t baramins be easily distinguished?
Taxonomy at the organismal and morphological level might be justified on phylogenetic grounds, but at the molecular level, it is a different story.
Taxnomic differences create nested hierarchies based on structure when we are talking molecules. That is unavoidable because of the discrete nature of chemistry and quantum mechanics and other physical considerations. The most blatant groupings are obvious starting with the periodic table of elements, but it continues with all the way to macro molecules like proteins.
There are 4 levels of protein structure:
1. primary – the amino acid sequence itself
2. secondary – simple structures like helices and strands
3. tertiary
4. quaternary
Many protein fragments having hardly and sequence similarity (primary structure) have the same secondary structure, especially things like an alpha helix.
But for starters look at the groups of Beta structures which are defined by structure, not by phylogenetic methods. Macro-molecules are better classified by structure and function. This will automatically create TAXNOMIC nested hierarchies at the molecular level. There is no need to invoke phylogenetic taxonomies, and by way of extension no need to resort to phylogenetic explanations for such nested hierarchies of structures. So for starters, the Beta class of secondary structure taxonomies:
Click here for an enlarged image:
http://theskepticalzone.com/wp/wp-content/uploads/2017/11/beta_taxonomy.png
What taxonomies? Nothing in your post made any sense. Literally.
ROFLMAO
I didn’t characterize Rumraket’s comment either way. That’s all on you, or rather your fevered (and usually incorrect) interpretations of what my motivation was.
Indeed.
😮
stcordova,
Sal, you really need to work harder on making your points clear and comprehensible. That read like gibberish. Now, I think it really was gibberish. But I might be wrong, and there’s no way to be sure unless you try to be clearer.
Jock:
You characterized it both ways, as I already showed. Which is it, counterargument or ‘supporting data’?
Good grief, Jock.
Yikes! Only keiths could, when challenged with “I didn’t characterize Rumraket’s comment either way. That’s all on you, or rather your fevered (and usually incorrect) interpretations of what my motivation was.”, respond with a link to his fevered (and largely incorrect) interpretations of what my motivation was.
Curious that it is keiths, and keiths alone*, that gets into these deranged pissing contests with other posters. It’s almost pathological.
Still not ready to “move on” and discuss your disagreement with John Harshman’s statement, I guess…
*Sal does deserve an honorable mention here, however.
Its a great article is it Alan?
An article about the best strategies to try to “win” arguments with creationists is a “great” article according to Alan. You love these kinds of things don’t you?
How can we spin the best. What’s the best way to use guerilla skepticism. How can biased hack moderators help in the ideas war. These are Alan’s paragons of propaganda.
NOT what is truth, but how to “win”.
That is why you are the moderator that you are. Why you couldn’t possibly leave your post until Lizzie gives you the all clear, stand down good soldier! “We will never surrender!”
Jock,
You got caught changing your story in order to cover up a mistake. That’s embarrassing.
Good luck trying to spin your dishonesty as if it were my fault, somehow.
I thought so. I thought Kane made some excellent points that you don’t have to attack religion or religious belief in general. His example of Ken Miller, a Catholic, who can hold to his faith while pointing out the absurdities of Creationism is a good one. It’s the same as the Dalai Lama stating religious dogma can’t be defended against scientific reality. Religion has to accommodate new discoveries.
A won argument is one where participants learn something new.
A 4.75 million year old Earth is not propaganda. It’s a verifiable fact. I didn’t think you subscribed to YEC beliefs about a 6,000 year old Earth and a literal Adam and Eve, global flood and a real ark.
Well, science doesn’t deal in truth or certainty. But it can challenge ideas that run counter to evidence.
One can infer common descent of what to a virtually total certainty?
Chimps and humans share 98% genetically. So it is 98% certain they share a common ancestor? If they shared only 95% would that reduce the virtual certainty?
Perhaps that’s an indication it should be read metaphorically.
keiths always has an advantage over teh rest of us due to his extensive and advanced training in mind-reading.
And of course, his claim that an argument can’t also be data is just absurd.
Why can’t it be both?
Good grief, Jock.
So does science.
Mung,
Sure. I thought that would go without saying! 😯
Mung,
Careful, Mung. That would spoil Jock’s argument.
Yeah, good grief, Charlie Brown, indeed.
It’s even sadder if you look at the context in which I made the statement that keiths is all exercised about. Well, that and his inability to distinguish between the links (data) and the linked comments (maybe data, maybe counter-arguments, maybe both).
Counter-trolling him is too easy. We should probably lay off, but the Lucy Van Pelt aspect is just too appealing.
I’m a bad person. 😉
False bravado, Jock. I doubt that you’re fooling anyone.
This is getting surreal. Jock writes:
He is actually trying to claim that the links themselves — not the linked comments, nor the contents thereof, but the links themselves — are ‘supporting data’ for his counterargument.
“Here are some links. You don’t need to click on them. The fact that they exist supports my counterargument.”
Jock, you must be really desperate to make an argument as pitiful as that.
Are you ready to admit your mistake yet?
The point was major macro molecule families like proteins are classified by structure and function and not by supposed phylogeny. I was beginning to make my case from first principles starting with the periodic table, then the secondary structures like Alpha Helices and Beta configurations in proteins.
There are 4 levels of protein structure:
1. primary
2. secondary
3. teriary
4. quaternary
From the structures in each of these layers we can synthesize a Linnaean like Taxnomic Nested Hierarchy based on physical properties like structure and function.
There are situations where differing phylogenies can arrive at the same taxonomic protein, therefore the Taxonomic Nested Hierachy of proteins is not generated by phylogeny, it’s the way the nesting would naturally happen based on structure and molecular behavior alone.
Below is one such nested hierarchy I posted earlier. It’s obviously not defined in phylogenetic terms but more like the Linnaean approach based on structure. If you think a little more, you can see where I might be going with this.
http://theskepticalzone.com/wp/wp-content/uploads/2017/10/figure31.png
LMAO
You give up too easily. Carry on. Don’t let me stop you. As Corneel pointed out, you might learn something.
Why? Harshman’s logic sounds good to me.
I provided a diagram of the G-Coupled Protein Receptors family (CCPR). It is noteworthy that phylogeny isn’t used to define the nested hierarchical structure of the members of GCPR family. See for yourself:
https://en.wikipedia.org/wiki/G_protein%E2%80%93coupled_receptor
I just showed then a Taxnomic Nested Hierarchy that is completely definable independent of phylogenetic methods. In fact, given some GCPR classes don’t even have sequence homology, one could see it is possible for different phylogenetic paths to lead to molecules in the GCPR family. Hence membership in GCPR doesn’t necessarily mean a GCPR protein is the product of common descent from some Universal GCPR ancestor.
As Linnaeus and the Creationists and Owen defined homologies and similarities in terms of platonic forms, this is exactly the way protein taxonomy and the nested hierarchies in the protein families are defined.
My point is that conflating the nested hierarchies of phylogeny with the nested hierarchies of structure-based taxonomy is a no-no. And in terms of operationally useful priority, structure-based taxonomy takes precedence over phylogenetic classifications. Further, phylogeny doesn’t generate such nested taxonomic hierarchies, since functional and structural hierarchies transcend common descent.
At the level of protein secondary structure, consider the alpha helix or the beta configurations I showed earlier. Many amino acid sequences can create such structures, they are not created by common descent but by the physical properties of the molecules. Independent evolutionary paths can converge and create alpha helices with totally different sequences. By way of extension then, the taxonomic nested hierarchy is not created by common descent, it is a common structural architecture, dare I say, common design.
Regarding why I believe the fossil record is young…
First, it takes a miracle for the Cambrian era to be real because of the Faint Young Paradox. Without the miracle of some fine tuning with Global Warming or Solar behavior, the Earth would have been an iceball during the Cambrian era, maybe even today.
The discussion was here:
The is C14 in diamonds and marble and various fossils including coal in the carboniferous. The presence of unracemized amino acids is also evidence the fossils are young. The erosion rates would have wiped out the geological column in several million years. Further the contact domains between strata are too smooth and the difference between strata sediments are so discrete, it doesn’t look like it was piled up over millions of years.
I also provided evidence of “ancient” bacterial DNA looking like the modern DNA in this thread. I just don’t believe the fossil record is young.
Further, I think the natural direction of evolution is reductive, not constructive, therefore time and millions of years really doesn’t help evolution.
Ergo, I accept common design via miraculous special creation over common descent.
That’s funny. Looking at the European Bioinformatics Institute’s page on protein families, we find it saying:
Margaret Dayhoff, who pioneered gene families in her Atlas of Protein Sequences in 1965, defined them by making phylogenies connecting their members.
That’s what the website claims, but I provided what actually happens in practice, namely proteins are classified by structure and function. The evolutionary claims are superfluous.
Here is one example of hierarchical classification of G-coupled proteins that don’t involve phylogenetic methods:
https://academic.oup.com/bioinformatics/article/23/23/3113/291144/On-the-hierarchical-classification-of-G-protein
I mentioned the sequence differences in proteins are not to be trivialized.
Before we invoke the hypothesis that most of the proteins can evolve mostly by random walks of functionally irrelevant mutations, we might want to wait till we learn more about the functional significance of sequence differences between these proteins. It’s a little hasty to assume the sequence differences have no meaning.
Just to get a flavor of how critical individual residues may be, see the discussion of motifs in these GCPRs:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885203/
Here is but a mere sampling from the above paper:
So what is the point of me mentioning this. Evolutionists want to argue the diagram below is from common descent from an ancestral GCPR protein via mostly random mutation that causes the descendant proteins to phylogenetically radiate into the various GCPRs below.
In light of the above citation, how hard does that look now given so many individual residues are functionally important? The residue differences could be functionally important in a species specific manner. We really know a lot less than the popular press would have us believe.
What did I say earlier about the importance of individual residues which evolutionists like Allan Miller think can just change so easily without functional compromise.
I mentioned the following post translation modifications on proteins that constitute some “-omes”.
Phospho proteome
Methyl Proteome
Acetyl Proteome
Glyco Proteome
Here is a paper on GCopuled Proteins known as Rhodopsins. See for yourself the importance of individual residues, some of which involve the above “-omes” I just mentioned, and then some.
That’s why I don’t think Theobald’s “random mutation” model of phylogeny holds much water in light of the functional constraints we are now becoming aware of on individual residues on a protein. Like I said, the substitutions can’t happen willy-nilly without functional compromise. How can a GCPR like Rhodopsin evolve from some ancestral GCPR given the functional importance of its individual residues.
http://www.sciencedirect.com/science/article/pii/S0014579301023924
Notice there is a species specific functional difference between the utilization of a single residue, Asparagine-8, between octopus and mammals and frogs! But its not just a single residue that is in question. Contrast the locations of the glycosylation sites in the Octopus Rhodopsin (at position 8) with that of Drosophilla Rhodopsi (positon 20 and position 196).
https://www.sciencedirect.com/science/article/pii/S0014579398001604
For chemical modifications to land in the right spot there needs to be an addressing scheme, which is most likely the sequences themselves providing road signs (aka binding sites) for molecular machines that make such postranslation modifications.
This is why the protein sequences count, they don’t just randomly mutate without consequence, and that’s why I don’t think they can just naturally radiate into a phylogenetic hierarchy without guidance.
ffs Sal, it’s like you have some sort of template you try to follow when you post, to make it appear as if you have a clue. Any given post should contain:
1. A list of some fancy, “cutting edge” technical terms.
2. A quote from a reference/citation.
3. A picture with a graph or diagram of some sort.
4. Mentions of titles, prestigious institutions, and journals.
It’s honestly pathetic. You just blather on and on following this fatuous posting template. It’s a form of spam.
Rumraket,
It’s pitiful, isn’t it? I suspect Sal himself is bedazzled by those things, so he assumes that his audience will be, too.
Moving on from DNA_Jock’s surreal CYA argument regarding links, let’s talk about the fourth comment, which, in his revised story, is the one containing his actual argument.
I wrote:
Jock, in the fourth comment, actually confirmed that:
Hence his links to three comments making that same point — a point that I had never disputed, and one I had made myself. (That’s the mistake he was trying to cover up when he recast those three comments as mere ‘supporting data’.)
No, I am considering the entire picture — guided evolution as a whole.
Descent with modification does not, in and of itself, produce a “mind-blowingly powerful phylogenetic signal”. Other conditions are required. This is a crucial point, so please ponder it.
Right.
To say there’s “a lot of signal” is just another way of saying that there aren’t too many anomalies.
Guided evolutionists need to come up with a theory that not only predicts an ONH; it also needs to predict one of the kind we actually see in nature. That requires assumptions that they, and you, can’t justify.
That’s incorrect. Where did you get your insider knowledge of the guider’s psychology? What entitles you to say “I know the guider would not act this way unless he were deliberately trying to obscure the phylogenetic signal”?
Humans routinely evolve their designs in ways that wreck an ONH. Do you think that in doing so, they’re deliberately setting out to obscure the phylogenetic signal?
It is you. You are assuming that the guider would behave in a way that would produce an ONH of the kind we see in nature. By contrast, I’m simply assuming that guided evolution would be evolution that is guided. Such a process does not predict an ONH of the kind we see.
Hence my disagreement with John’s statement…
…and your echo of it:
A “context of common descent” is not enough. Other assumptions are required, and those assumptions are not justifiable.
stcordova,
I’m not talking about protein trees. I’m talking about species trees, or at least what SINE data may tell us about them. I have been talking about SINE inserts, and only SINE inserts, for several pages now. I’ve been sat here calmly as you flurry about in a maelstrom of point-missing and misdirection.
Now, SINEs. They are used to assess familial relationships. Also relationships among species. So at what taxonomic level does the logic break down?
stcordova,
Yawn. As I’ve said time and again, the fact that some sites may be under constraint does not place all sites under constraint.
Hey, let’s look at the pattern in a non-coding region, shall we? Let’s look at … I dunno …. SINE inserts? How come clades share these? Any idea? I have …
stcordova,
As I’ve said, transposition is not evenly distributed along the genome. It happens most in actively transcribed regions, because that fraction is most accessible. If Rat and Mouse euchromatin map reasonably closely (as they might in these related, commonly descended species), then there’s a sound reason you might see coarsely parallel frequency.
I don’t see how this supports Common Design either way. A genetic element whose ‘prime directive’ is to transpose does not need to be stuck in place by a Designer! There is a clue there.
John Harshman,
Granted, though I acknowledged that in the parenthetical comment immediately following – the more sites you pick, the more clearly homoplasious anomalies stick out as noise among the signal.
And anything at all that’s not explained is a miracle.
Of course that is the central fallacy of ID, and it is incurable among its internet supporters.
Glen Davidson
Wow, that took longer than it should have, really.
True that other conditions are required. Specifically, imperfect DNA replication, and death.
No it isn’t. What a lame rhetorical gambit. Consider four generations of a homothallic yeast: there would be one glaring anomaly (they switch mating type) and not a lot of signal (maybe a handful of mutations). Potentially problematic for a phylogenetic analysis. In contrast, consider a million generations: maybe in addition to the mating type anomaly, there’s an HGT event. Doesn’t matter, because there’s thousands of mutations, which form an ONH, i.e. a “lot of signal”. Wouldn’t matter if there were multiple HGT events, thanks to some asshole with a pipetteman, it’s the “lot of signal” that allows the statisticians to do their thing with confidence.
How about “To say there’s “a lot of signal” is just another way of saying that there aren’t too many anomalies, given that there’s a lot of signal.”? Not quite as zing-y, tho.
[I can head off goofy crap too: at a given signal:noise ratio, confidence increases with the amount of data.]
Absolutely correct, they do, and I wouldn’t even try. Care to retract your claim that I was supporting guided evolution? I thought not.
No, I do not; but I don’t think that they are designing within a context of common descent — the people who try to draw that lame-ass analogy are, well, y’know, IDists…
Oh-err. I think the penny has finally dropped. I don’t need to assume that the guider “would behave in a way that would produce an ONH of the kind we see in nature“, I just need to assume that the guider “would behave in a way that would produce an ONH”, that is, does not intentionally destroy the massive signal.
It’s not the existence of an ONH that argues against guided evolution — it does not — rather it is the precise nature of the ONH that we do observe that betrays no detectable hint of guidance, when certain categories of guiders (e.g. the ones that theists hope for) would be expected to leave a detectable trace within the ONH. There are, of course whole categories of guiders (matchmakers, cullers, and experimentalists) who would leave no phylogenetic trace whatsoever.
As mentioned above, imperfect DNA replication. Not really an assumption. Here goes: “I assume that life and death are old, and DNA replication has always been imperfect.”
John wrote:
He did not say “the precise nested hierarchy that we observe”, he said “a nested hierarchy”, I said “…if this guiding occurs within the context of common descent, then we would expect it to produce an ONH.” You read something into these statements that was not there. You’ve been tilting at windmills.
Now, perhaps I could have pointed this distinction out to you earlier (John actually did, but you appear to have missed this), but you seemed so gosh-darn eager to pick a fight. So some counter-trolling may have occurred. I am a bad person. 😉
So after the mouse/rat clade diversified into mice and rats, it was then that the retro elements (B1/B2/B4 SINE for mouse, ID SINE for rat) started to get inserted in the same places. That hardly seems like a set of random events, 300,000 of them in independent lineages. So why didn’t it happen before the split? Your explanation isn’t mechanistic, it’s an ad hoc apologetic.
If you bothered to read and comprehend the work of an evolutionary biologist like Sternberg on the evolutionnews weblog you might appreciate the point being made and why your dismissive ad hoc fix to the problem looks like something concocted rather than systematically considered.
Sternberg:
Btw, Ayala’s understanding of Alus is obsolete. He fails to appreciate the 100 million A-to-I editing locations that Alus generate in the transcriptome which even biochem textbooks are reporting as likely functionally important.
Feast your eyes on the correlation of SINE positions in Chromosmome 10 in the mice and rats. How’s that for common design independent of common descent. Yeah baby. That’s a common design pattern independent of common descent.
This pattern which Allan Miller finds so trivial, was not viewed that way by the Director of the NIH and the former head of the human genome project. Nooo, what is one Darwinists trash is another’s remarkable treasure.
So Allan, if the director of the NIH and former head of the human genome project found this pattern compelling, maybe you shouldn’t be so dismissive of it as you are now.
We are finding function for these SINES. For example, they delimit the chromatin extrusion loops. Did they just pop into the right place by accident too?
stcordova,
Hey, I wonder if these SINE elements themselves appear commonly descended on sequence criteria? I wonder how they got in the clade in the first place? Anyhoo …
All you have is a coarse pattern – a graph of frequencies covering many megabases. If you have more detailed evidence that the insertion points are precisely the same, I’d like to see it. Otherwise, I suspect a coarse mechanism, such as following the euchromatin. Have you properly considered that possibility, like a good scientist might?
You seem to be using the word ‘random’ to mean ‘not planned’. Is that the case? Me, I mean (in this context) ‘equiprobable’. No, insertion is not equiprobable, for the reason I have already stated twice now – euchromatin. Random … it’s one of those words that cause a lot of cross-talk, and I think you could find a less ambiguous word to make your meaning more explicit.
Why should it? Not everything is obliged to occur prior to a speciation event. What a curious question.
Bollocks. Euchromatin is more accessible to transposons than heterochromatin. That is mechanistic.
Pause for a hearty chuckle. Aaand …
My suggestion is not exhaustive of mechanistic possibilities, but it is a real and known constraint upon transposons. They do tend to occur in transcribed regions; I didn’t just make that up. Also, they tend not to occur in actual ORFs, for obvious reasons. If the coarse gene/intergene and chromatin patterns of rat and mouse genomes has been retained, approximately, guess what I’d expect to be guiding transposon clustering? So this pattern could readily be confirmation of common descent! I’m not going to do any work to prove it, of course, but then all your are doing is riding on Sternberg’s coattails yourself.
Meanwhile … well, what’s your explanation, again?
stcordova,
Hee hee, an argument from authority. You know there are authorities that consider common descent to be universal, and common design a heap of crap, don’t you?
Beyond the correlated patterns between mice and rats, we see correlated patterns between mice and men. The Alu-like patterns Sternberg refers to are the mice B1/B2/B4 SINES and the rat ID SINES.
Sternberg points out:
Sternberg writes regarding the chromosome banding patterns
But, ahem, how do we have “conserved” banding patterns that happened after all these lineages split?
https://www.researchgate.net/figure/51713113_fig2_Figure-6-Conservation-of-chromosome-banding-pattern-between-mammals-A-Conservation-of
So did these bands conspire to appear AFTER the lineage splits? That’s not consistent with random mutation, and it is especially bad if we discover these SINES and LINES have functional significance.