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.
How is “an out of space time design” in any way simpler than common descent? How does it better account for the data, unless your argument is that a miracle can account for anything at all with equal probability? And how, I repeat, does this account for the nested hierarchy pattern in the data?
Simpler, in the sense of merely utilizing your preconceptions.
How does that account for anything at all?
Glen Davidson
Examination of Evidnece pro and con for Common Descent:
nested hierarchical patterns in trees buitl with individual genes: PRO, good
Conflicting nested hierarchical patterns in trees built multiple genes: not so good
orphans sytems: HECK NO, CON
pan-genome (“flower diagram”): suggests genome destruction, not construction, CON
results from phylogenetic methods: too much uncertainty, conflicting and fudgeable results, not so good
Conclusion: Common descent is hardly a convincing theory relative to something like the theory of Maxwell’s Equations in Physics of electricity, magnetism, and optics. If people want to believe it until the day they see God working miracles, I respect that, but I just don’t find the theory able to explain what it claims to explain from first principles of physics and chemistry and math.
stcordova,
Judging by your lack of arguments for it, common design has absolutely nothing going for it, with, of course, the lack of homologies past the point of apparent divergence arguing strongly against.
Blather on with your lack of understanding of common descent all you want, common design doesn’t even start to explain anything.
Glen Davidson
Sure. Why the surprise? 🙂
This is not really the appropriate thread to discuss this. I´ll just note that the popgen cannot be blamed for the poor survival of highly ornamented birds.
You can´t blame everything on evolution you know.
Hey, not my claim. I am just trying to figure out Sal’s argument.
An “out of space time design” is simpler? LOL
Corneel,
If I were a hardcore materialist I would agree with you. 🙂
John Harshman,
How do insist on a nest hierarchy pattern of genes for common descent when Rumrakets model shows rapid genetic divergence after only a few simple cell divisions?
The pattern staying common after many generations is evidence of design.
Your only evidence of conflicting patterns so far is your little COX I tree. Is that really a fair test? And I have already pointed out several crucial problems with your analysis.
You must offer some kind of argument rather than just this nod toward an argument you have never made. What orphan systems are you talking about, and how do they argue against common descent?
How does this suggest genome destruction rather than construction? Again, you must make an explicit argument rather than just waving in the general direction.
Another unmade argument. What counts as too much uncertainty, and how do you know? What conflicting results? Most especially, what is this accusation of fudging, and how can you back it up?
You will first have to figure out what the theory of common descent attempts to explain, which you have not yet managed. The first principles are simple enough: a history of branching descent accompanied by mutation and fixation within populations. Note that the causes of mutation and fixation are not featured or necessary to the theory. So, how do you explain the nested hierarchy of life?
I don’t know what you mean by any of that. Please try again.
I would agree the absence of erasure is evidence the patterns of diversity have been constrained. One really sees this with bacterial genomes that should be totally mangled by now such as with the aaRS gene and which, due to their large population size can’t be explained by coalescence. Alternatively, as in Rumraket’s case, the number of generations was limited, meaning the age of the lineages wasn’t that great. So alternatively one could argue the INTRA-species lack of divergence is evidence of the youth of life — Young Life Creation.
The nested hierarchies that are ATTEMPTED with protein phylogenies. They aren’t very definitive. The ones with Orphan Systems are very much more powerful.
Simple example:
Humans nest within Primates, Primates nest within Placental Mammals, Placental Mammals nest within Mammals, Mamalls nest within nest within Vertebrates, Veretbrates nest within Eukaryotes
This can be done without protein phylogenies as Linnaeus did simply with Orphan features.
One minor technical note. John Harshman asked why I didn’t just use Genebank to assemble homologs, but used Psi-BLAST instead. I replied I wanted to be extra careful to get the best possible homolog in species, because I didn’t always trust the annotations. And indeed I’m finding this to be a good approach.
For example I had a species of bacteria that had identical proteins listed in GenBank under two totally different names and catalytic functions! This is a result of the way gene predictions work and the different models employed by the sequencing centers.
Out of all I’ve said to you, you pick this one trivial point to respond to? Some might consider that avoidance of the real issues.
Why? And what are “Orphan Systems”?
Please name the “Orphan Systems” that define each node within this nesting. And why does this nested hierarchy exist?
Seconded. I’d like to know as well.
Corneel,
I’ve explained Orphan Systems many times, and if that didn’t suffice I provided examples of them. John is on my ignore list because doesn’t expend much effort to understand.
So here is the response I feel he deserves:
http://orphansystems.com
No.
In real biology, the genes are much much larger, sit in much larger genomes, and the mutation rates are much lower. In my example, I simply “sped up” evolution so divergence became apparent.
But this very thing is actually stacking the deck in the favor of making the hiearchy more difficult to detect. ¨
The very small genes I made up (20 bases), and the very high mutation rate (each copy event introduces a mutation in the gene), radically increases the odds of both convergent evolution and reversal (two lineages independently had the same mutation happen). Both of which are factors that confound phylogenetic analysis.
Despite radically increasing the odds of both convergent evolution and reversal as compared to real biology, we still got three highly congruent trees that also closely resemble the real phylogeny, even thouth there were over two million different possible trees.
Your intuitions about this whole subject keeps being completely wrong Bill. And for these reasons, everything Sal agreed with you about, above, is also diametrically opposite to demonstrable fact.
Then you’re an idiot and are obviously just running away from the most competent criticism you’re getting around here. Truly pathetic.
Besides, regarding making an effort to understand what you say, it is you who should be making an effort to express yourself clearly and correctly. You and Bill have gotten into a habit of just blathering and stuffing your sentences with technobabble neither of you half-way understand. Of course, by doing that, you can avoid having to make concessions about things you’re wrong about, and make it seem as if there is some sort of high-level technical debate going on. When mostly it’s John trying to explain something to you and get you to really address the subject of the nested hiearchy, and you just blurping out random technical jargon to keep up appearances.
I know, but those explanations suggested different understandings of the term. I have taken it to mean general apomorphisms, ORFans, taxonomically restricted genes and complex molecular networks. That’s quite a mixed bag. This is why I requested clarification.
You have put John on your ignore list? The one person that, after Joe, is most competent to judge your dabblings in phylogenetics? That’s ridiculous Sal. I advise you to reconsider that decision.
+1
Corneel,
In deference to you, Corneel and Rumraket, I’ve taken the resident Phylogeneticist, John Harshman off ignore. I didn’t put him on ignore because he lacked expertise, but I thought many of his criticism were extremely petty and tiresome and didn’t add to my learning.
I spent over one-hundred dollars on Joe Felsensteins book and even more money to study under a computational evolutionary biologist and an expert researcher at GenBank, and I try to slug through Joe’s writings probably as much as any one here at TSZ.
John was right and pointed mistakes I made about:
Cox1
NJ being an approximation of Least Squares Fit, not exactly a Least Squares Fit
multicellular creatures not being a taxonomic group
some interpretation about the numbers on a bootstrapped diagram
The rest I felt mostly misrepresentation of what I said, and taking time reading responding to John felt only a fraction as productive as reading Joe’s book and associated papers and authors referenced by Joe. Maybe the only thing all of us can agree on is Joe’s books would be valuable reading for everyone in this discussion. The two are Theoretical Evolutionary Genetics (free) and Inferring Phylogenies.
In any case, I mentioned Orphan Systems was my phrase expanding the notion of Orphan Gene since Orphan Gene is a more modern term, but this is more like an expansion of a Taxnomically Restricted Gene. The better systematic term might be the various kinds of APOMORPHIES which I’ve mentioned in this discussion, but there are all these subtle definitions Hennig put together which strike me more like the evolutionary version of what Linnaeus did better without any evolutionary assumptions.
I described systems like the spliceosomal intron system. I find it annoying to discuss whether to define it an Orphan System, an Apomorphy, Synampomorphy, Plesomorphy, set of Oprhan Genes, set of Taxonomically Restricted Genes, a derived character, a shared character…. whatever. That sort of gets in the way of analyzing the complexity of the system.
If advocates of universal common ancestry find Spliceosomal intron systems insufficient evidence against common descent, then I respect their freedom to believe what they want, but that whole system looks to me like it doesn’t have an ancestor! If there is common descent, it seems a statistical miracle was needed to make the insertion of that system possible. Yeah, we can make phylogenetic diagrams of the shared proteins in all domains of life, like Cytochrome-C or maybe aaRS, but the genes coding these proteins have a different architecture which I showed in part with:
most prokaryotic versions of the gene
XXXXXXXXX
most eukaryotic versions of the gene
iiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiii
In addition to that I could discuss different ribosomal binding sites between the two like Shine-Dalgarno in the prokayrotes vs. the variety of others like Kozak consensus in the Eukaryotes. But these get hand waved away and instead of focusing on the mechanistic difficulties, I get repeated questions of what do I mean by Orphan Systems.
If you want me to spell out what I’m referring to. maybe I’ll just call it “Sal’s ever expanding list of systems that defy Universal Common Ancestry” of which the Spiceosomal Intron System will be at the top of the list. There are big difficulties like this, but lots of other small ones.
One long term project I’m envisioning is the study of the question I posed regarding the aaRS gene. There are papers indicating there is observable decaying codon bias in microbial genomes. If the codon bias doesn’t recover, this would suggest real-time genetic entropy in the microbial genome and suggest life on Earth is young. The problem of microbial pan-genomes is real as well.
So as far as this thread goes, I might share some of the gene trees I put together. Regarding E. coli, Salmonella, Streptococcus whatever, all these pathogenetic bacterial have like 50,000 different genomes sampled for all the strains and patients and places where they were extracted. YIKES. I’m not after building phylogenies for them, I want to see how detectable the genetic entropy is on them.
John Sanford’s group has kept a passing eye on the DE-Volving codon bias in microbes such as these. Divergence patterns in aaRS is an idea I kept bumping around with the other’s in John Sanford’s group and outer circle (like Nathaniel Jeanson). I may post what I come up with now and then on those topics….
stcordova,
Sal, in all that long screed you failed to define “orphan system”. You gave a couple of examples, but, absent a definition, I would need many more examples before I was confident of your meaning. Specifically, you mentioned that humans, primates, placental mammals, mammals, vertebrates, and eukaryotes are each defined by orphan systems. What, in each case, are the orphan systems you refer to?
Speaking of Inferring Phylogenies, have you come to the place where Joe cites me yet?
Good, I think that is a wise move.
We all feel like that about some commenters on this forum. But, as long as they are not being abusive or obnoxious, putting people on ignore goes against the spirit of TSZ, I feel.
What is “decaying codon bias”? Taken literally, it would seem to mean evolution toward a more even distribution of codons used for a given amino acid. That would be weird if true, but I don’t see it as a problem for old life. What do you mean?
@John. You owe us a beer now.
What is interpreted as adaptation, if irreversible in the population may be codon bias decay (compromise of function). Here is an example paper:
http://jvi.asm.org/content/89/21/10762.full
John Sanford and Rob Carter have also published on Influenza viruses, so I think that’s how the issue came to their attention:
This is the popular version:
The peer reviewed paper by John Sanford and Rob Carter is here:
https://tbiomed.biomedcentral.com/track/pdf/10.1186/1742-4682-9-42?site=tbiomed.biomedcentral.com
The book has an index, so it is possible to find the citation. John was cited concerning a claim he had made, in a dispute over the validity of bootstrap methods in analysing results from parsimony methods. And I agreed with John’s work, because it was well-thought-out and valuable. He is well-educated and knowledgeable on phylogenetic methods (and on vertebrate phylogeny more generally). He knows what he is doing.
Add in his labors here and on other blogs (Sandwalk and Panda’s Thumb, for example) where he rarely loses his temper in spite of enormous provocation. We all owe him a debt for outstanding public service.
stcordova,
Sal, all that tells me nothing. Please try again. What is “decaying codon bias”, and how does it argue against old life?
The paper you linked to is about codon bias evolving to fit the host and engineering of codon bias. The quotes don’t even mention codon bias except for (apparently) a tendency for H1N1 to drift away from human codon bias patterns. But this is an extremely short term effect, not something that could have been happening for thousands of years (except, of course, as a series of repeating processes, but in that case it could as well have been happening for millions of years).
No. But since Joe just paid you tribute.
page 345:
and the citation
Thanks, Corneel, Rumraket, and Joe. But will Sal ever address any of the major questions? Especially, will he ever tell us how common design explains the nested hierarchy of life?
Ok, then I’ve told you nothing. Maybe there is little point in you saying anything because you’ll just claim I told you nothing. But in deference to Corneel and Rumraket, you aren’t on my ignore list. But, I’ll just continue to tell you nothing, and you’ll just continue to listen to me tell you nothing maybe for the next several thousand comments at TSZ. Surely you can find more valuable ways to invest your time than me telling you nothing like:
I thought your response was lame just like your response about Spliceosomal introns. But that’s my opinion. Since I think it would be so nice of you to give Corneel and Rumraket a beer, I will however keep you off my ignore list.
Thanks anyway for your response. Maybe next time you can provide something more substantive than a glib dismissal and complaining I told you nothing.
stcordova,
Once more: how does “decaying codon bias” argue against old life? Rather than launching into a diatribe, why not try to communicate clearly and answer questions?
John,
You asked:
I felt I gave you a good answer to that question as to what I meant. Whether my hypothesis is true or not, I thought my response was clear enough.
I thought Rob Carter and John Sanford at least outlined one line of bio-informatics research that could be pursued.
Regarding Young Life, that’s a separate question, but I took exception to you saying that I told you nothing when I cited relevant papers especially from two YECs who published in BMC that I felt answered your specific question about what is codon bias decay. Sanford and Carter used the word “erosion”. My term “decay” was consistent with what they were trying to communicate.
Sal, I don’t think anyone is trying to be obtuse or anything here. Seriously, I’m trying to understand what argument you’re making here about codon bias and it’s really not obvious to me how this is in any way a challenge to life being old, or the nested hiearchy.
Please, please make an effort to really spell out the logic of your reasoning. If X -> then Y. Because X is three times more likely than X1, and X1 bla bla bla. Put some meat on your arguments. Don’t just cite stuff and then pretend you’ve done some sort of work.
H1N1 influenza virus displays a move away from a codon usage bias general to the human population… therefore… what? I’m missing the actual reasoning here. You pick some rather obscure fact. Then you state a conclusion. But where is the connection between the two? Why does it follow, or perhaps why is it more likely, that life must be young, because of the codon usage bias of H1N1 influenza virus?
I’m having trouble understanding this codon usage phenomenon in H1N1. If it’s consistently moving away from host codon usage patterns, how did it get to using the host pattern in the first place? Given the time scale, this is clearly not something that happened during Creation Week. It has to happen within a human generation or so, repeatedly.
Rumraket,
The way you phrased things is something I can work with. However, I take exception to Harshman saying I told him nothing. I sometimes assume too much as far as everyone’s understanding of phrases being thrown around. Harshman could admit he’s unfamiliar with a concept that YECs are quite familiar with, and a concept that is peer reviewed papers published by evolutionists! He could admit that rather than say I told him nothing, especially after I take the trouble to provide citations of that idea in peer-reviewed papers that specifically used the phrase “continuous erosion over time of codon-specificity ”
But to your question, codon usage erosion suggests that there might be some functional ideal that can be deviated from. Codon usage bias is a well-known phenomenon, especially in bacteria. Granted viruses aren’t bacteria, but we might learn something from them.
So one theory is natural selection maintained codon bias. [If so, how then can synonymous mutations really be neutral? but I digress.] If codon bias is also eroding in some lineages, then natural selection isn’t maintaining it, in fact some of the papers argue natural selection is changing the codon bias as a means of adaptation!
The point I was making by citing codon usage changes in real time (as in less than 100 years) is genomes in microbes can diverge rather rapidly. We are seeing real-time detectable changes. If we clock this rate of divergence, whatever number of nucloetides per generation, we have a molecular clock of sufficient accuracy may to ask questions about the age of life.
In other words, over time, we should expect groups of organisms like say E. Coli or whatever to have substantial divergence between the members of the group. John Harshman argued the lack of this divergence in genes like aaRS is due to coalescence, and I objected and said that for such astronomically large numbers of individuals spread across the globe, coalescence can’t explain the lack of divergence, Young Life is a better explanation.
The H1N1 work of Carter and Sanford was accepted because of its relevance to the pathogenicity of influenza, it wouldn’t have passed review if it were offered as evidence of YEC, but their policy (John Sanford’s group) as far as contributing to peer-reviewed literature is to provide papers that are relevant to operational questions such as the treatment and diagnosis of diseases, if it co-incidentally has creationist implications, then all the better.
When I met with Rob Carter (the co-author) at ICC 2013 (International Conference on Creationism), we talked about his paper and I told him about the lack of divergence in the H1N1 virus genomes as evidence of young life. He said that was an interesting question. We talked about purusing it, if not with H1N1, something else. The project has languished ever since, but it has been on my mind, and it was part of my motivation for studying bio informatics and Joe Felsenstein’s works…
But…..perhaps rather than following what I have to say, how about examining a paper where someone may be stating the problem better than I can. If one can’t see the problem he way John Sanford, Rob Carter and myself have expressed it, perhaps this paper might state the problem better!!!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC150674/
I posted this paper earlier. It was ignored. Maybe it’s worth discussing again.
stcordova,
Sal, I must ask you once again to focus on clarity, to make clearly expressed arguments for clearly expressed points. Your scattershot, digressive, rambling comment is not very helpful. How does “decaying codon bias” argue for young life, which was your original contention? How does rapid evolution in viruses, in general, argue for young life? In addition, how does the recency of various RNA virus families argue for young life? What you quote does not state the problem, if there is indeed a problem.
The paper provides at least three explanations for the apparent recency of RNA virus families, none of which is “young life”. It seems to have left out another explanation I would think applicable to retroviruses: that they spend a fair amount of time inserted into host genomes, during which time they evolve at the host rate. But what do you see as problematic about the explanations given?
Nothing yet, but if experience is a guide, I’ll find some just like I found the errors in Ohno’s work and just as I finding the molecular clocks don’t agree with the emergence complex orphan genes like those among the 200-300 proteins in spliceosomal introns.
But to your objection:
to which the author says regarding 2 of the 3 solutions:
But I really like what the 3rd solution:
Yeah. The recent origin of RNA viruses is that they are recent!
Like your glib disimissal of the problem of orphan genes like those in the spliceosomal introns that break the slow evolution needed to make gene tree phylogenies, you’re making a glib dissmissal of a problem I sense with the RNA viruses.
No need to settle the issue today. Unlike you who has a tendency to dismiss anomalies as minor, I’m rather interested in studying them. So if you accuse me of ignoring issues, I could point out the plethora of things you ignore that I put on the table that don’t fit so nicely with your models.
This is what I highlighted. You don’t see that as even hinting of young life. Ok. You don’t take hints very well. I also provided and example of ancient bacteria found in a salt fossil that had didn’t have enough divergence after supposedly 200 million years. You gave it another glib dismissal as a minor anomaly. You practically ignored the faint young sun paradox and the problem it poses for an old fossil record. Another minor anomaly in your eyes, but not mine.
We won’t agree on maybe a lot of things, but we can probably talk about gene sequences and how they compare and the reasons for their patterns of diversity and similarity. I can comb through gen bank and just report on the patterns of similarity and diversity. You’ll interpret it one way, I’ll interpret it another, but at least we can agree on how similar of diverse something is from something else. That’s about all we can productively hope to do.
For a change we may have some morsel to agree on. The un-inserted retro viruses have one clock rate versus that same virus when inserted into a host genome.
Hypothetically, some viral clock rates could be estimated for when they are free.
As far as influenza, there was an estimate of clock rates provided by Carter and Sanford comparing different strains of influenza.
As far as the Edward Holmes paper, we could hypothetically take the sequence divergence of the RNA viruses in question as far as what the inferred clock rate is based on how the RNA viruses diverge from each other, and then compare that to the clock rates of the RNA viruses diverging from their hosts. That’s an interesting application of the clocking math that has a bearing on Phylogenetic Inferences.
Maybe that’s one of the few productive areas of investigation worth pursuing coming out of this discussion on Common Design vs. Common Descent. I might contact John Sanford over this issue and some issues with Mendel’s Accountant after I clear some things off my to-do list.
So I’ll report back. There will be the 2018 International Conference of Creationism in August, so I think there will be a lot of YEC geneticists at that meeting. I can bring this issue up of RNA viruses at the conference. This could be an interesting question in its own right.
Sal, I implore you to try harder to focus on complete arguments and leave out extraneous points that come to you in the middle of something else. Both your recent responses could communicate as much on-topic at a tenth the length, and with greater clarity. I also implore you to make sure that the sentences you type make sense, both to you and to other people. Please take more care when composing your comments. Read them over at least once before posting. It’s a simple courtesy to others and a potential benefit to your reputation.
Now, let’s complete your quote-mine: “The final explanation for the recent origin of RNA viruses is that this is in fact what happened. The key to this hypothesis is that the molecular clock dates discussed throughout this paper only relate to the RNA viruses currently circulating, that is, those that have been identified over the last 100 years or so. Thus, RNA virus families like the flaviviruses may in fact have histories dating back many millions of years, but the early members of these families have gone extinct to be replaced by those we sample today. All that is left following these extinction events are the very long branches relating the different families of RNA viruses to each other.”
In other words, a form of coalescence, the frequent pruning of lineages. RNA viruses as a group are not young; discernible clades of RNA viruses are young, quite a different thing.
And finally…
I find your overwhelming arrogance to be one of your greatest sins, and exceedingly hypocritical in one who claims to be a follower of Christ.
The implication is these RNA viruses (not in a host) are young, or at least recently released out of some host.
That’s your circular reasoning again based on the assumption of universal common ancestry.
The evidence at the very least is an event happened that caused the free moving RNA viruses started diverging from a common ancestor recently. Agree or disagree?
No, that isn’t the implication. Are you sure you read the paper?
It’s what fits the data and the observed behavior of virus lineages. Remember the bit about H1N1 strains frequently going extinct? That will end up making the common ancestor of living strains much more recent than the common ancestor of all strains.
Disagree. What happened wasn’t an event; it was lots and lots of separate events happening frequently over the course of many years: strain extinctions. Are you sure you read the paper?
Thanks for the clarification, but I think you are making the discussion needlessly complicated. Here you appear to be saying that orphan system is your term for apomorphy. But in the five questions on common descent thread you contradicted this.
If both orphan systems and nucleotide / AA substitutions qualify as apomorphies, my comment was correct, and your objection just confused the discussion. You may argue that ORFans, TAGs and complex molecular networks cannot evolve by natural means, but that is another matter.
Still I implore you to use these terms. It clarifies your arguments and helps the communication. If you simply adopt the jargon you might find that John will stop hammering away at you asking for definitions.
Let me tell you something John, I was talking about some basic stuff about chromatin once at TSZ. I made the simple statement that there were readers, writers, and erasers for histones. You disputed that. I then pointed to peer-reviewed papers that showed this was a common concept.
We had several exchanges like that which made it shocking for me to find out you were actually a biologist because you didn’t understand elementary concepts. It became a little difficult for me to hold you as an expert. As I tried to educate you on this basic concept you kept presuming I was the one in error because I’m not a biologist. The same thing was happening in the Ohno thread. You presumed because he was Ohno publishing in PNAS and that I wasn’t a biologist, that I was wrong. To your credit you saw the light and finally agreed I was right, and Ohno was wrong, even though he is still cited by Ken Miller and evolutionary biologists on the topic of nylonases.
I still point stuff out to you and it just seems to float over your head and you pretend I didn’t catch your error. You argue doggedly for coalescence as an explanation for lack of divergence in populations with an astronomical number of individuals. Then you talk down to me like I didn’t catch you error. I provided you with papers that cited the coalescence time as it relates to the number of individuals, and then you say you don’t understand my point.
That’s a fair criticism, however, I thought the formalism of Hennig and the Phylogenetic Systematist to not be that accessible.
The term “Orphan Gene” is a play on words from ORFan (Open Reading Frame). It is a term in use today. There is also the concept of Taxonomically Restricted Gene.
The problem with Gene emphasis is that there are heritable features like glycans and structures (prions are the simple example) that are not genetic. I took a little flak at TSZ for pointing out some of the mechanisms of inheritance that are not genetic, but which are significant, are usually ignored because they are not single-point-of-failure systems like genes, thus their heritable nature isn’t obvious.
Thankfully, my mouth was empty when I read that.
Sal, you appear incapable of communicating clearly.
When scientists communicate with each other, they are careful in their use of language; when asked for clarification, they clarify. The entirety of your shtick, especially when it comes to biology, consists of fuzzy thought obscured through fuzzy language. For you, that’s a feature, not a bug.
When another poster points out one of your legion of misconstruals, you get all huffy and offended, asserting that any suggestion that you don’t understand X is obviously refuted by the fact that you “pointed to” X in a previous comment.
Guys like John, Joe F, and Rumraket have the patience of Job dealing with you.
The reason that we ask you to be precise in your use of language is the forlorn hope that, by thinking with clarity and precision, you might someday come to the realization that most of what you think is either incoherent or mutually inconsistent.
Your attempts to “educate” biologists about biology just showcase your inability to read for comprehension. You also appear rather insecure.
I have some issues I have with Hennig and the Phylogenetic Systematists.
First off, from a practical standpoint, in protein classification, individual proteins have secondary structures like alpha-helices which are structures shared by proteins that aren’t considered similar by homology but by convergence. It becomes a little cumbersome and unnecessary for most proteomic researchers and structural biologists and biophysicists to really care whether its a homology or homoplasy. An alpha-helix has certain geometry and chemical characteristics (like residues that conform to a particular Ramachandran plot).
Then there are things like motif and domains and folds. There are things like the zinc finger domain. Many proteins, IIRC, maybe 1% of all proteins in humans have a zinc finger domain. When is it a homology or homoplasy or apomorphy or synapomorphy that a protein has a zinc finger domain. Most structural biologists and proteomic specialists probably don’t care, and I don’t see those Hennigan terms hardly used at all in literature investigating the structure of proteins.
So when there are a set of genes shared only by a chicken and a human, what should we call those genes? Is taxonomically-restricted gene the correct term? I think “genes shared only by chickens and humans, or birds and primates” seems an accurate enough description. Frankly, I wouldn’t know what to call it in Hennig’s terminology.
How would we classify Zinc-Fingers in Hennig’s terminology?