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.
I understand that very well. It sounds fancy and technical, so is a nice rhetorical device that makes it seem as if Sal is really clued in
Ancestors of modern mammals are in effect said to be like the lungfish and coelecanths of today because lungfuish and coelcanths of long ago are very much like the ones today.
How do you find Orthologues for INF3/4 in primates, mammals and fish? Or, just as importantly, how do you demonstrate such orthologs don’t exist in certain species.
I don’t believe INFL is a mitochondrial gene since it resides on Chromosome 19. Learn some biology.
There is no such gene anywhere in the human genome.
Interferon lambda 3 = IFNL3
Learn some biology 😉
stcordova,
Izzatso? I dunno about that, but I do know that the genetic constitution of these species is not likely to be any kind of good approximation of the genetic constitution of the common ancestor of coelacanths, lungfish and ‘other fish’. Coelacanths et al are not genomes preserved in aspic; they are likely to have evolved approximately as much as we have, genomically, from that common ancestor, even if they are morphologically little changed from fossil exemplars. People take this ‘living fossil’ stuff far too literally.
Sal, If you are going to condescend, it works better if you are not wrong.
In addition to mangling the name (IFNL3/4) of the gene on Chr 19 that you are attempting to look at now, you missed the fact that John was referring to your previous attempts, which used the mitochondrial gene Cox1 (that’s cytochrome oxidase, although you thought you were looking at cytochrome c).
See how it’s done?
Well, the old-fashioned way would be to extract some DNA, construct a set of primers, and do PCR. Not every gene for every species is in GenBank yet. You could try in silico PCR on the UCSC genome browser for those species with genomes already done. Mostly, you seem to have recovered ESTs, and your probe sequences seems much longer than the gene you’re searching for if gene predictions are correct.
Then again, why should I help you when your go-to response is “learn some biology”? Aren’t you the expert, apparently?
Two problems. If we don’t know what the constitution is (initial state), we have no business guessing how it goes from the initial state to the final state.
Next, according to the cherry picked genes used to build phylogenies, the assumption is the initial state is similar enough to the final state we can make phylogenetic estimates, which means the genes don’t evolve so much that they stop being BMP2, Cox1, INFL, etc. homologs after millions of years.
At best, one can say they just find a trajectory believable, but one can’t argue from any sort of first principles of statistics that POOF-omorphies like INFL are the expected outcome of an evolutionary process. They might only be able to argue a gene shared by a set of species evolves by slow enough amounts of change they can be argued to be homologous between species.
Those same statistical arguments for slowly evolving genes, if extrapolated to Taxnomically Restricted Genes, totally fall apart. Hence, we have at least two nested hiearachies. The nested phylogenetic hierarchies defined by shared genes (and conflicting at that), and the nested hierarchies defined by unshared genes and morphological characteristics.
If hypothetically I asserted common descent, I’d say mammals and fish are sister groups descended from a common ancestor that wasn’t exactly like either of them. The prevailing claim is that mammals and other tetrapods descended from a fish-like creature rather than some unspecified vertebrate. I would, if I were assuming common descent, argue for an unspecified vertebrate for the origin of mammals, not a fish.
No, I’m not an expert, but you represent yourself to be one. You’re an expert in your field, I acknowledge that.
Why do you need a gene prediction to search nucleotide sequences? You yourself said to include the introns, so why do we need a gene prediction in other species to see if a known DNA sequence in humans has similar orthologs in other species? Shouldn’t a nucleotide search of a statistically complex (aka non-repetitive) string catch a similar nucleotide in another species?
I was able to fudge the search rather easily by taking the translated protein and putting it in BLASTP. I found lots of candidate orthologs that way. But that sort of masks the degree of evolutionary change that is really taking place. That is cherry picking. When I built a tree on the proteins rather than the entire gene, I got a different looking tree. That’s an illustration of cherry picking.
Then stop asking me to “learn some biology”. You think I don’t know which genes are mitochondrial and which are nuclear?
You don’t. I merely point out that what you claim to be the sequence of a particular gene actually seems to be far larger. It’s useful to know what you’re dealing with. And introns have nothing to do with it.
This is just some bullshit you make up because you don’t understand that you pick the genes most likely to be phylogenetically informative. That’s not cherry picking, it’s making sure your job isn’t harder than it needs to be.
As an analogy, if you wish to measure the distance to the peak of some mountain from the base, you don’t pick the most winding, circuitous path up the mountain to perform your measurements. If at all possible, you want to perform a straight line measurement.
Avoiding mitochondrial genes, or fast-evolving immune-system loci or what have you, is not to cherry pick. It’s simply to avoid making a job you know is possible to do, harder than it needs to be.
What you need to explain, and you have not even attempted to explain, is why there EVEN IS any amount of such congruent phylogenetically informative genes, that together with morphology, all significantly corroborate each other.
No amount of you coming up with examples of a phylogenetically uninformative locus is going to make the informative ones not exist and demand a scientifically falsifiable and sensible explanation.
You lost this one, and it’s been over since 1859.
You mean the ones that agree with forgone conclusions. Why not start with the genes that don’t exist in one group but exist in another. The least-squares fit should be freaking obvious in that case which set of taxa should be aggregated with another set of taxa. You’ll get a different tree if you do it the right way, that is because it is from a wholistic representaitive sample, not a cherry picked sample.
I mentioned the challenges the phospho proteome presented to the algorithms that underlie phylogenetic gene tree building. There is a rather naïve assumption in phylogenetic gene tree building that there isn’t a lot of functional compromise or variation in the process of evolving homologous genes.
Here is a sampling of the post-translational modifications on Topoisomerase II in yeast vs. humans. This was gleaned from an informational report I sent to a Topoisomerase researcher recently. It’s easily constructed from Uniprot data. Anyone can assemble such a report on any gene:
Or, if he has moderator privileges, he’ll delete the entire thread and all your hard work when things start to go south on his arguments. Speaking from experience, here.
How would that be able to tell whether they share a common ancestor?
You can very likely find genes not shared among two arbitrarily picked people on Earth. Does that mean they don’t share common descent?
It is entirely possible there are cells in your body that don’t share genes. Some might even have remnants of viral infections you’ve suffered throughout your life. Does that mean those cells did not descent from the same zygote?
With these simple examples it should be obvious that mere presense-absence of some collection of genes can’t in and of itself determine whether two organisms share common descent.
If you weren’t the kind of guy who is actively seeking a particular conclusion you desire, but were instead thinking about what common descent would actually imply (and what would follow or not follow from alternative models), you’d have been able to figure this out for yourself.
Least-squares fit is the Sal Cordova fancy technical term of the month it seems. A few weeks ago it was Hidden Markov Models. Before that it was something about post-translational modification with polysaccharides (“the sugar code”, “glycome”, etc. etc.). Then there was all that shit about read-write RAM, and chromatin parking spots and bla bla bla.
Only the most gullible and ignorant sycophant is impressed by your ability to copy-paste technical jargon.
How do you know whether you have a “wholistic representative sample”?
FWIW, there reason for interest in the phospho proteome of Topoisomerase is the issue of targeted chemo therapy for cancers.
Topoisomerase inhibitors are a means of killing cells. We do know that the phosphorylations turn on and off various proteins, and also the patterns of phosphorylation are cell and tissue specific. Some of the nastiness of chemotheraphy might be alleviated if the phosphorylation patterns can be manipulated in a cell type and/or tissue specific manner.
In the process of looking at this, as an academic curiousity, it is evident “higher” eukaryotes like humans have a far more complex implementation of Topoisomerase than other creatures.
Hahahahaahaha. Speak of the devil… “phospho proteome”. Ooh that’ is SO fancy and technical sounding. And it ends on -ome. What a buzzword!
Look at this completely uninformative, brainlessly technobabbling and pretentious bullshit.
You are such a goddamn fake.
You wouldn’t know academic curiosity if it sat on your face and tried to auto-erotically asphyxiate you.
Please stop this pretentious bullshit you utterly transparent con-man and charlatan. Shouldn’t you be out preaching a prosperity gospel? I’m sure you can lure a few dollars more out of Bill Cole.
Ok, we can go simple. Mammals have mammary glands, fish don’t. Placental mammals have placental mammalian placentas, fish don’t. You distinguish one group from another based on things one group has and the other don’t. That includes genes like Interferon Lambda.
Vertebrates share genes and morphology that unifies them as a group. I have no problem with that. You can arranged the vetebrate groups into nested hierarchies. I have no problem with that.
However, if you start cherry picking genes and morphological features that are only shared between members of the group and totally ignoring features that are unique to a group (like INFL) — I have a major problem with that. When one cherry picks data like that, one gets different nested hierarchies. It’s ok to get different nested hierarchies. It’s not OK however to pretend that’s the ONLY nested hierarchy possible. It’s not OK to fail to point out when the data sets had some heavy cherry picking away genes that were present in one group and absent in another.
You are using word you don’t understand to make yourself seem sciencey. There can’t be a least-squares fit in the absence of a sequence. You can’t do any kind of sequence analysis in the absence of a sequence. Nor does anyone pick genes that agree with foregone conclusions; after all, you can’t tell whether they agree until you do the analysis. And you have no idea what “the right way” would be; you lack the knowledge and, apparently, the interest in learning.
Sure there can. If a primate has INFL and a fish doesn’t, you fit the primates together to the exclusion of fish. No problem. You just can’t arrange the fish in a hierarchy based on INFL, but you know then a primate isn’t a fish, contrary to Axel Meyer’s claim “we’re all Sarcopterygiian fish”. No we’re not, not relative to INFL genes and maybe a whole lot of other ones.
Sure you can say the lineages gained and lost genes. But then, those are ad hoc rationalizations as to why the data don’t agree with foregone phylogenetic conclusion. So the phylogenetic tree ends up being built with whatever ad hoc rationalization needed to arrive at a foregone conclusion. You can do that, but lets not pretend such methods are comparable to the methods that vindicated Electro magnetic theory. Not even close.
Well, I’m glad to see you’re reading my posts even if you don’t respond, and have figured out that there are fish with placentas. You have not so far determined that any species lack interferon lambda genes, just that you have trouble dealing with GenBank.
Why don’t you have a problem with that? How is it explicable under your creationist paradigm?
What evidence do you have that “one gets different nested hierarchies”? So far you have managed to look at a tiny taxon sample of two genes, COX I and some nuclear gene I disremember. The latter gave you the standard tree, while COX I gave you a problematic tree. All you have after that is a meaningless accusation of cherry-picking that you can’t back up. And you can’t analyze sequences that don’t exist. Now you can code them as missing data, and this is what we do. Feel free to try that.
All you’re doing here is demonstrating that you don’t know what a least-squares fit is. If you were capable of embarrassment, that should embarrass you. And you don’t know the distribution of “INFL genes” within vertebrates either. Stop making things up, and start learning the meanings of the terms you toss around.
All you are demonstrating here is that you don’t know how phylogenetic trees are built. That too should embarrass you.
stcordova,
I don’t know what is achieved by such volume dumps. Some sites are modified. That may be a constraint on those sites. So what?
stcordova,
Sigh. No-one has made any attempt to guess how it gets from that state. What are you reading? Certainly not what is written.
Hmmm…a quick and cursory google, the sort of thing Sal should be doing before spouting off, at a minimum. Shows that inferferon-lambda family genes are widely distributed in amniotes and that zebrafish have an apparent ortholog. Now will he be embarrassed? Probably not, since mistaking COX I for cytochrome-c didn’t embarrass him in the slightest. Incapable of shame.
stcordova,
Hang on – even if that were true, why are there any genes that ‘agree with foregone [descent] conclusions’?
Here’s a starter: I can look at genes held in common between Common and Spotted Sandpipers. Is it reasonable to say that sequence commonality indicates common descent at that level, or not? If not, why not, and what is it instead?
Of course it indicates common descent. Because they are the same “kind” and descended from the same pair that rode on the Ark. Once they left the Ark, they quickly speciated and natural selection (and the other usual evolutionary forces) differentiated them into the Common and Spotted Sandpipers in just a few dozen years.
You know, the same evolutionary forces that Sal has argued so strenuously don’t work. There is the after-the-Ark exception that comes into play.
No, it’s more like determining whether French and English are related, or what manuscripts are related. Which can be done to very high levels of certainty.
And yes, you compare related words, not the ones with unknown etymologies. No sense to that, of course.
Languages and manuscripts don’t fit into nested hierarchies as well (unrelated stuff gets into them more readily), but of course there’s really no question about the related nature of English and even Hindi.
But you whine about methods in biology that are more rigorous than the methods used to compare languages and manuscripts, without a cavil against linguistics and stemmatology. Any good reason for that?
Glen Davidson
Rumraket would.
Every time he knows.
It happens daily. 🙂
And that has have provided with a nice example for the most obvious question: What prevents us from classifying organisms on the basis of having a placenta, or having “ovaries” or having sonar, or any other convergent character ever brought up here by creationist commenters? Any classification system has become completely arbitrary and subjective. In Sal’s system, mammals no longer exist as a subjective entity, but only by the grace of prioritizing “mammary glands” over some other trait (placental mammals are grouped by having a “placental mammalian placenta” heehee). Yet he maintains that the “taxonomic hierarchy” is real. How so?
This!
This we should be discussing.
To any anomaly, we can ask the same question: what makes you think it is an anomaly?
Creationists tacitly acknowledge the overarching pattern even as they try to deny it.
Cordova’s Law: the amount of ‘cherry-picking’ one must do in order to find genetic commonality increases proportionately with increasing divergence between genomes. I can think of at least one excellent mechanistic explanation for this curious phenomenon.
More importantly, you have no explanation for that.
Glen Davidson
Of course, not only has Sal not explained the derivative nature of classification, he’s not even begun to try to explain (or more likely, obfuscate) why the temporal dimension of groups like mammals reveals the same evolutionary branching. That is, why don’t we see mammal fossils 200 million years ago, but do see cynodonts with their interesting homologies with mammals, like the synapsids with their intermediate auditory ossicles? Then eutheria appear around 160 million years ago, and slowly begin to increase in species numbers. After the K-T extinction event, especially, they adaptively radiate into over 5000 species.
Same story of evolution told through history as told by classification today. Branching off into separate clades is shown both through time and via distinct characters in present-day species.
And Sal just has “goddidit” and ‘miracles did it because evolution couldn’t.’ It would indeed be a miracle that not only a frozen snapshot in time reveals the patterns expected from evolution, but so do the appearances of fossils through time, without, of course, it all happening according to evolution. But I guess if conjuring up miracles is all that you can do, you may as well do it across the board.
Glen Davidson
Let’s remember that Sal doesn’t believe in any time series, since the stratigraphic sequence came about in a single year of violent flood. There is no “200 million years ago”, just the year of the flood. So he really needs to explain why the flood stacked up fossils in a sequence that corresponds so well with a nested hierarchy. But Sal is unwilling to discuss flood geology. He won’t even commit to a spot in the sediments that constitutes the end of the flood, which one would think would be obvious.
John Harshman,
Yes, he won’t really discuss any of the colossal failures of ID/creationism, but just reacts against evolution.
That’s the cul-de-sac that ID/creationism always ends up at, however, since it’s a complete non-starter for supplying any kind of real answer or science project.
Glen Davidson
And why all these mechanisms of “poly constraint” operating on genetic sequences to prevent evolution, somehow weren’t in effect post-flood just so all the “kinds” could massively radiate into hundreds and hundreds of distinct species for the still thousands of “kinds”. In virtual hyperspeed evolution.
But all of that is irrelevant, because he’ll always just say “god did it”. And while he may deny it in so many words, he affirms this in practice:
I have it on good authority (Professor Byers) that the top of the Flood sediments is the K-T.
Nested hierarchies defined by POOF-omorphies aren’t the same as the conflicted cherry-picked nested hierarchies defined by gene trees supposedly created by slow evolution. Therefore God created the nested hierarchies defined by POOF-omorphies because evolution can’t.
The first POOF-omorphy listed was the spliceosomal intron system. Within vertebrates, there is the problem of mammary glands that define mammals. Veretebrates are generally defined also by insulin regulated metabolisms. None of those are even remotely explained. The gene trees I’ve shown are conflicted and cherry picked, and thus don’t always agree with the POOF-omorphy trees. Case in point: giraffes aren’t fish.
I’m having a problem assembling a set of quality orthologs of Topoisomerase IIA.
Funny how you can’t find any significant examples of those. Your most egregious examples of conflicting trees were constructed by picking mitochondrial genes and comparing their phylogenetic trees to nuclear genes, for taxa that share common descent something like 450 million years ago. And still the number of incongruent branches were ridiculous insignificancies. A lesson you seem completely unable to fathom. Not to mention how you constantly fail to account for why there even is any congruence at all.
You know, that whole thing about the Consilience of independent phylogenies.
As has been repeatedly demonstrated throughout this thread, all your creationist rationalizations about “design plans”, “common design”(which you can’t even define what is supposed to mean), or “poly contraint” instantly collapse under first scrutiny.
“Game over, man. Game over!” – Bill Paxton, Aliens (1979).
As usual, the explanation for the origin of a clade-defining character is evolution by natural selection, mutation, genetic drift, speciation and so on and so forth, while the explanation for it’s distribution in groups within groups, is common descent by a branching genealogical process.
Not only is it explained, it has been fully and thoroughly explained since 1859:
“…So that we here have many species descended from a single progenitor grouped into genera; and the genera are included in, or subordinate to, sub-families, families, and orders, all united into one class. Thus, the grand fact in natural history of the subordination of group under group, which, from its familiarity, does not always sufficiently strike us, is in my judgment fully explained.” – Charles Darwin, The Origin of Species, 1st Edition.
How about INFL? What does your gene tree look like with that one. You want some more, we can try building them. We have lists of lots of genes in mammals not found in fish, and vice-versa.
Oh, I know, you’ll come up with an ad hoc rationalization of adding and deleting genes in each lineage. But that’s an ad hoc rationalization of a gene tree conflict fixed by cherry picking, it’s not saying the conflict doesn’t exist. The fact you have to cherry pick genes that exist in all the lineages is a problem with the method, it’s not a problem with the data. The data which say a gene exists in one lineage and not in another tells you the lineages are far more distantly related than suggested by focusing only on shared genes.
I mentioned INFL which is part of the primate immune system. Primates are part of the mammalian group.
Mammals have a different immune system then fish. It should be no surprise then mammals have a genes that are different than fish. It seems that if one wants to conceptualize legitimate nested hierarchies, one builds them based on similarities and diversities. A system or gene existing in one group that doesn’t exist in another is a basis of defining these groups as distinct.
The mammalian immune system (among other systems) defines mammals as distinct from fish. Therefore, Axel Meyer is wrong. We’re not Sarcopterygiian fish, because Sarcopterygiian fish don’t have mammalian immune systems. Hones gene trees will reflect this.
http://www.els.net/WileyCDA/ElsArticle/refId-a0001284.html
stcordova,
Fer God’s sake Sal, you take the both. How many more times? It’s not just the identities, its not just the differences, it’s the pattern.
stcordova,
That’s just nonsense. Sarcopterygians all have the same basic adaptive immune system, fish to mammal to reptile, etc. Of course the mammalian immune system has evolved, as no doubt has the fish immune system, but there’s no large difference between any of them.
You have to go to the agnathans to get a substantially different adaptive immune system.
Glen Davidson
Yes, and the pattern says mammals aren’t fish contrary to some of the gene trees that phylgeneticists mangage to concoct..
Evolutionists keep arguing the gene trees always have congruence with the morphological and physiological nested hierarchies. That’s not true. In fact, the gene trees don’t agree with each other if one takes into account the genes missing in one lineage and present in another.
I’m merely pointing out the incongruence between the nested hierarchies generated by different methods.
Unlike Casey Luskin and other IDists, I’m not saying nested hierarchies don’t exist. In fact I argue, like Michael Denton, that nested hierarchies exist according to the typological (rather than evolutionary) view of nature. The typological nested hierarchy doesn’t agree with the evolutionary nested hierarchy. Ergo, giraffes aren’t fish.