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.
John Harshman,
If enough data is collected it will tell us the expected variation in genetically related organisms. If then Joe takes comparative data on the 3 sparrows there is something to compare it to.
You are assuming what you want to show, that genetically related organisms can only have as much divergence as can be found within populations. What if there were a greater divergence between two sparrow species than between two humans or dogs whose pedigrees you know? What would that tell you?
John Harshman,
I would like data on humans dogs and other species where we know ancestry exists. If Joe’s sparrows fell within the range of variation exhibited by the DNA results I would call that a positive test for common ancestry.
I would also like to know what would be evidence for “whole cloth” (aka “poof”) origin for any species.
It’s more like a culture thing. As a matter of culture, I expect you to have a reason for what you are saying. What you say has to be leading somewhere. It has to make sense in context. It’s not nice to throw random questions into air.
Because, apparently different from you, I feel responsible for my words. I have no clue about sparrows. I don’t know them. I can’t talk about what I don’t know. I know dogs and wolves. But if both dogs and sparrows can serve the same purpose in the dicussion, why did you not accept my answer?
You mean back when I said (to Allan Miller) “..reproduction is not common descent..” I was making a false distinction? In response I got assertions that evidence for speciation etc. is not required to demonstrate common descent. But there’s no reason why you should follow my exchange with Allan.
You have not directly admitted it, but when you say for example, “The fact is, we can’t even conclusively tell whether two fossils belong to the same species, because the idea of species we generally use is all about reproductive compatibility, and that’s the sort of character that isn’t generally preserved in fossils” then there are not too many ways to interpret this.
And this insult shows how biology works? It demonstrates how species evolve? Can you stay on topic?
“Inference” by itself belongs to abstract sciences only, like mathematics. Maybe the sort of biology you do is purely abstract. This would explain completely why you fail to understand what is being asked when you are asked about causes and observations, repeatedly over and over again.
Gosh, and I thought there was a field called “statistical inference” where they (we, actually) analyse data from science. That includes John Harshman’s work in molecular phylogenetics.
But now we’re told that this inference stuff is only for abstractions, and not actual data?
Yup, this explains it.
Statistical data is an abstraction. It entails no causes by itself.
And with that, Erik has discarded pretty much all of modern science. We infer a causal relationship because we give one set of patients a drug, and another set of patients a placebo, and observe that the group given the drug exhibits some change not seen in the placebo group.
The cause is inferred to be the drug, but it’s not like we have little cameras inside their cells that can really see the molecules and what they do.
We have a theory about how the drug might work, and tests of various sorts have been done designed to eliminate or minimize the effect of other contributing causes. But it’s all inference. Compare the predictions of theories with observations, infer a casual relationship.
So Copernicus’ inference that the Earth revolved around the sun from his observations was wrong or simply not an inference? Or are you saying that he was observing abstractions?
Incidentally, there is an entire field of assessment known as inductive reasoning, which is (in case you were unaware) inference based on observation. You might want to look into it…
Yes. But a statistical inference is a logical and mathematical inference. What it concludes, is a probability. So this is consistent with Erik’s remark.
But what we infer is a statistical conclusion. Our conclusion is that a particular therapy has a significant probability of a beneficial effect. This does not actually contradict Erik’s point.
I tend to see it as a proposed convention. I’m not a historian of science, but I somehow have the impression that Copernicus never claimed it as an inference.
I haven’t done any such thing. My questions do lead somewhere, but you are unwilling to follow. I take it that you are unwilling to believe that two species of sparrows are related to each other until such time as I can show you a movie of one species (though they need not be sparrows) turning into two species. I take it also that you may have a definition of “species” and a definition of “speciation” that differ from those used by biologists. Hard to tell, because most of what you say seems to me incoherent and off point.
What sort of responsibility does that entail? It doesn’t seem to be a requirement that you make sense, or be clear, or talk about something you know anything about.
Let’s not fool ourselves. You have been talking about what you don’t know from the beginning. Dogs and sparrows can’t serve the same purpose, because I’m trying to find out if there are any two species you think are related, and you don’t think dogs and wolves are two species, just one. Still, we can get something out of it. What makes you think dogs are descended from wolves and that dogs and wolves are one species?
No, I mean that “reproduction is not common descent” is nothing like “Evidence that those sparrows are related is not evidence that all life is related, or even that all sparrows are related. You need different evidence for different things.” You seem to have completely misunderstood my statement. Evidence that those sparrows are related would be the pattern of similarities and differences between those species and other similar species of birds. Evidence that all life is related would be the pattern of similarities and differences in all life. Those are different sets of evidence, but they are certainly similar sorts of evidence. What you demand is simply senseless.
Perhaps there aren’t many ways to interpret it, but you seem to have hit on a nonsensical way, though I can’t quite figure out what that way is. I’ll just say that what you quoted there is nothing like an admission that I have no relevant evidence. It’s a comment about what can and cannot be learned from fossils, but it has nothing to do with what can be learned from phylogenetics, or whether we can have evidence of speciation, or whatever else you think it is.
First, it isn’t an insult, merely an evaluation of your understanding of science. No, it doesn’t show how biology works, in particular, it shows how all of science works. All science is inference from observation. It’s common for creationists to treat “inference” as a pejorative term, as you do here. But that’s a rejection of science and of scientific methodology. And yes, inference from data is how we can know how species evolve. You have been informed about the data and about the means by which we infer from those data how species evolve. You just reject the inferences because you don’t like them. But you can’t explain any flaw in the reasoning.
Yes, that’s why we’re always talking about inference from data, not just inference by itself. You have been shown plenty of data and you have been shown the reasoning that leads to inferences. All the inferences of evolutionary biology are firmly grounded in data. Now what you want to see is something other than the data we have, and it’s something we don’t actually need.
If I confess to having no idea what you’re talking about in the last several posts in this thread, will you explain?
Fair enough I suppose. Rheticus states that Copernicus’ heliocentric model was the result of inferences based on comparing Urania’s guidance and assessments (in addition to Copernicus’ own observations) with Ptolemy’s hypotheses. Perhaps it’s a quibble, but I submit that not all inferences are based on abstractions.
Perhaps a better example is the inferences that come about in forensic science. Inferring where a shooter was standing based on where a bullet or casing is found doesn’t strike me as a result of abstract data. But perhaps I don’t know what Erik’s concept actually is.
It was related to Erik’s comments about inference. I often disagree with Erik, but he was right that the technical meaning of “inference” is really only applicable in abstract logical arguments. However, people do also use “infer” in an informal and non-technical sense, where Erik’s comment does not apply.
If “infer” isn’t the proper technical term for what scientists do with data, what is the term?
The claim that the data sets are independent is, of course, quite nonsensical.
Silly me. I thought the fact that my siblings and I share the same parents was proof of common descent. God I feel stoopid now.
What makes these data sets independent, especially given the theory of common [dependent] descent?
We can build genealogical trees because we know how people are related. It has nothing to do with this phylogenetic nonsense.
Scientists do infer.
In a strict technical sense, they make an inference in their model. But when they interpret there model to reach conclusions about reality, then that interpreting is not inference (at least in the technical sense of the term).
It is common to be a bit casual in talking about that — as long as Erik isn’t watching.
Neil Rickert,
My thoughts are that an inference is the first step in forming a hypothesis, Once the inference is made then you test it to validate the hypothesis. In the example that Rumraket cited he is referring to the 4th or 5th round of validating the hypothesis with phase 3 human trials.
In the case of general relativity an inference was made from a thought experiment of a light shining through the hole in an elevator and bending as the evaluator accelerated at close to the speed of light. Since there is mathematical equivalence between acceleration and gravity the inference was made that mass was not attracting objects of mass but bending space time as it was affecting the trajectory of a massless object, light. His first step after this inference was to build a mathematical model. Then the predictions of the model were tested successfully several times.
Neil Rickert,
Thanks, but that doesn’t answer my question. What is the technical term for interpreting a model to reach conclusions about reality?
colewd,
Then why don’t you accept something similar with regards to phylogeny? The model of common descent predicts nested hierarchy in data, and this has been tested many times with all sorts of data.
The claim was that it predicts the actual data, not just any old data. If it works with all sorts of data then it predicts pretty much any tree you can imagine.
How do you know which tree is the correct tree? You don’t.
John Harshman,
I do accept it at some level. The question is where is the line of demarkation? How much genetic variation can be generated by reproduction?
Common descent proposes reproduction, isolation and the variation that goes with it as the cause of new species. I agree that descent would predict a nested genetic hierarchy relationship but we see other issues in the data.
Instead of a tree lets call it Sal’s flower. We don’t have evidence that reproduction can add or subtract genes yet this is what Sal’s flower is telling us. We also don’t have evidence that reproduction can change splicing codes.
How did around 10,000 pseudogenes in the human genome arise? You know, things like yolk proteins, cytochrome c, and many others.
You have the strangest notion about how genes can’t be lost, despite a huge number of pseudogenes that exist. Of course you can’t explain that by design–or anything at all–especially things like yolk genes, but evidence doesn’t have a great effect on you either way. Not on this issue, anyhow.
On the gain side we have many protein families, yet you claim that we have no evidence that reproduction can cause the gain (no, I’m not interested in “mechanisms” that have no evidence for such “causes”). It’s just evidence you don’t like that must be considered dubitable, and anything said by a creationist who can ape a few big words counts more than any knowledgeable person’s statements.
Glen Davidson
What makes you think there is a line of demarcation? What would prevent any given amount of genetic variation from being generated, given time?
No, common descent doesn’t propose a cause of new species. Common descent proposes separation and divergence, but speciation is another matter. If you agree that common descent would predict a nested hierarchy, then why do you doubt tests of common descent through discovery of nested hierarchy?
Yes, we actually do have evidence that reproduction (by which presumably you mean mutation) can add or subtract genes. I’m not sure what you mean by splicing codes, but wouldn’t they involve changes in DNA sequences, which is what mutations do?
John Harshman,
Several issues but an example is Sal’s flower. I don’t think genetic variation from reproduction can create that pattern of added and lost genes. Genes lost in two linages is a complete show stopper for me.
Would it be fair to say common descent is a claim that the diversity we see is caused by reproduction and its associated variation?
I think the observation of a nested hierarchy does not isolate common descent as the only cause. The observation of the data in Sal’s flower trumps the nested hierarchy observation.
I have yet to see any that is convincing.
Why, and why? You may think it’s obvious but I assure you it isn’t.
I think it’s a bad way to say it, but it isn’t entirely wrong. The simple word for what you say here is “mutation”. And of course diversity is caused by mutation, fixation, selection, perhaps species selection, and the wide variety of environments available.
Why does it trump nested hierarchy? How is it even incompatible with nested hierarchy? And what is the alternative cause of nested hierarchy?
I suggest that polymorphisms within a single species ought to be such evidence; would you agree? If we can find a species, some members of which have a gene and others of which don’t, would that be good enough?
Similarly, I have no idea why you think the different sparrows you refer to are different species when Chihuahua and St. Bernard’s are one. Despite multiple attempts to get you clarify what species means, you are not even understanding what is being asked. So your question about sparrows remains futile.
Now, I get that the term species has multiple aspects and can be approached from many different angles. But surely there is one or max two angles relevant for the current purpose. I keep highlighting the one angle I know – interbreeding. Occasionally I get ridiculed for that, but I would appreciate it if those more knowledgeable here would highlight other relevant angles, you know, even if just to show that you in fact are more knowledgeable. Unfortunately you are so infatuated with your particular science that you have lost the ability to distinguish relevant from irrelevant, to boil a subtopic or a term down for lay audience, things like that.
As if your science were the only one. There is a difference between biology (a particular science) and science in general. But, as said, you have lost the ability to make relevant distinctions. I happen to be a scientist in my own field. I know where it begins and where it ends. Whereas you think that those who are not experts on your particular field know nothing about science in general.
The relevant distinction is inference based on a (scientific) model versus observation about reality. For example, people (let’s label them “population”) breed more people (let’s label them “fertility”) while other people die away (let’s label them “mortality”). Statistics is a count of each of the three labels. Statistics is just numbers and the science of statistics is to look at the (cor)relations of these numbers. Across time, those numbers change, increase and decrease. However, the numbers breed nothing. The numbers have nothing causal in them. This should be crystal clear as soon as we make the numbers to be about anything else, say, dashes on a sheet of paper. The causality is (may or may not be) in what the numbers are *about*, and they are *about* an observation about reality, in this case “people breed more people while other people die away”, which is completely independent of statistics. For the said observation to apply, nobody needs statistics.
So observation about reality is one thing, scientific model (which may be about whatever part of reality or it may be abstracted so many levels away that everybody has lost clue what it is about) is another thing, and the connection between reality and the model may or may not be there. Just like there are false analogies, there are false scientific models. I am not saying your model is false. I am saying that you are taking your model for reality. You have lost the sense of orientation. You are speaking in the model’s terms when my question is about biological reality.
I have only been asking: What is the causal link that justifies the assumption of common descent? This is not a statistical question. It is also not strictly a genetics question. It is a question stemming from the biological fact that species breed the same species, so how does the variety of species come about to the point that they lose the ability to interbreed, e.g. apes and humans are said to have common descent, but do they interbreed? Why (not)? What is the cause? This is categorically important in order to figure out what genes do, not just what they look like in different species.
But I have basically given up hope to try to find ways to get useful information out of you.
Not correct Mung.
It is of course true that they’re not independent from the standpoint of descent. Which is the whole point of phylogenetics.
They’re not independent of descent, which is why they can be used to extract the genealogy of the organisms. But their sequences are independent of each other. In other words, you would not expect that if you built a tree using one gene, and compared it to a tree from another gene, to yield a highly similar tree unless they went through the same genealogical process. It is exactly because the only sense in which they aren’t independent is through descent, that they can be used to infer the line of descent.
Let’s say you want to try to estimate a phylogeny for some collection of very widely divergent species. You pick two genes for that, like cytochrome C and ribosomal protein L14p. Those two genes have their own sequences, and they’re independent of each other. As in, the gene-sequence of cytochrome C is not causing the gene-sequence of L14p. Nor is L14p causing the gene-sequence of cytochrome C. There is no nucleotide-to-nucleotide (or amino acid to amino acid at the protein level) relationship between any two nucleotides, or amino acids, in these two genes.
There is no relationship between them that says that, if the cytochrome C DNA sequence has a T at position 24, then so will L14p DNA have a G at position 13 (or position 1, or 2, or 3, etc. etc.). Nor someting like it for amino acids. A glycine residue in cytochrome C at some positoin will not be causing there to be a valine residue at some position in L14p. Or any other “connection” you can think of. The sequences do not cause each other.
So if two mutations have happened in cytochrome C over some stretch of time, you would not expect the two mutations in cytochrome C to also cause there to be two mutations in L14p.
So the only “connection” there actually is between them, is that they go through the same line of descent. It is because of this shared descent that you predict they should yield a highly similar phylogeny even though you have these two genes in many wildly different species.
I’m sorry but this is just false. We can built phylogenies for individual human families* by using loci of known high variability. You couldn’t built a phylogeny for a human family (like you and your immediate ancestors and siblings) by using cytochrome c, or ribosomal proteins. Or indeed almost any protein in the human genome, because they’re much too conserved on so short timescales. They’d be completely identical in nearly all cases, so they give no genealogical signal.
But there are such things as high-variability loci in the human genome, where there are measurable changes from one generation to the next. It is regions like these that are used to estimate relationships in DNA-based paternity tests. And they really can be used to built a family-level phylogeny.
* Not to be confused with the cladistic or taxonomic rank “family” used in cladistics and taxonomy.
Has Mung explained why he accepts common descent when he rejects the very best evidence for it — the objective nested hierarchy?
This makes no sense at all. The statement “this has been tested many times with all sorts of data” is just saying that there are many types biological data that gives phylogenetic information.
Before DNA and protein-sequence based phylogenetics, they used various forms of blood-test and immunological (cross-reactivity of antibodies for example) data, besides the usual comparative morphology.
You seem to think “all sorts of data” means “data from any imaginable object, biological or not”.
Hey let me google “estimate species tree”.
Estimating species trees: an introduction to concepts and models.
Not that your question is even relevant, because we technically don’t need to be certain that we have found the true species tree, in order to be justifiably certain that the species in question share common descent.
Also, the level of certainty associated with any particular tree estimation comes in degrees. It is not some black and white dichotomy where we either know with absolute certainty what the true tree is, or we don’t know it at all. It doesn’t work like that.
Erik,
Evidently, deaf as a post.
Erik,
Loving the haughty cluelessness!
Newsflash Erik, cytochrome c is not the only gene ever sequenced. My question related to the point (using one protein as an example) at which common descent shades into common design, not that cytochrome c is itself evidence for common descent. There must be some point in the series where it it is inherited from a common ancestor by 2 individuals, not ‘designed into them’.
Allan, re Erik:
When you wish to remain a creationist, it’s best to deflect evidence before it gets into your brain.
John already mentioned it, but evidently it needs repeating: speciation is not assumed in phylogenetic models. It just requires lineage splitting and divergence, which occurs whenever there is reproductive isolation ( let’s say a mountain range or a wide river separating two populations).
Well, can you answer: What do genes do? What made you single out that particular gene? What does it represent? How does it prove your point?
Biologists here seem to not understand these questions (because it turns out they are actually statisticians). If my questions happen to be inapplicable to biology, can you tell why?
keiths,
That’s certainly writ large in the responses to this. The paraphrases of the opponents’ positions are teeth-gratingly bad, and telling. Almost as if there is some kind of Demon at work.
For example, the point I made about cytochrome c (which I didn’t even bring into the discussion), and where in the taxonomic series we elide from Common Descent to Common Design on % identity, comes back mutilated as “Allan says cytochrome c is the evidence for common descent”.
But since you are hung up on speciation: populations lose the ability to interbreed whenever they develop epistatic interactions that are incompatible in their genomes. This is the subject of a huge body of research, so nothing mystical going on here.
Since you crave for some “useful information”: The classical model that describes how this may happen is the Dobzhansky-Muller Model.
It goes like this: Suppose we have a diploid parental population that carries two genes A and B, with no variation. Like this: A1A1B1B1
Now the population splits into two, and although “species breed the same species”, within any species the offspring will be different from their parents (is that evolution you are talking about? yes it is!). In this case population 1 fixes an alternative allele at gene A (Let’s call it A2), whereas population 2 fixes allele B2 at the B gene:
pop1 : A2A2B1B1
pop2 : A1A1B2B2
Now this is all fine since A1 goes fine with B2, and B1 goes fine with A2, but whenever alleles A2 and B2 are combined, this results in a lethal combination. This effectively prevents population 1 and 2 from interbreeding, since the hybrids will combine the fatal allele combination:
hybrid pop1 x pop2: A1A2B1B2
Voila: speciation. Again a scientific model I am afraid, but one that is corroborated by observation from reality, since real world examples from such incompatibilities have actually been identified in species pairs. Usually the incompatibilities extend to more than just two loci, but the concept is quite sound.
Erik,
It was not even me that brought cytochrome c into the discussion. I forget who did; I’m sure you too have a functioning scroll wheel. But, given that cytochrome c had been mentioned, I used it as an exemplar to ask a question. I could have picked any other gene, pretty much, and asked the same question. There isn’t much point in repeating that question; you saw it and copy-pasted it once already.
I don’t know what you are saying here.
Corneel,
There is also the relationship between genomes in meiosis to add. Crossover siting is not totally ‘random’, but appears at hotspots, and effective synapsis and crossover resolution depend on high sequence identity – ie, a reasonably close genetic relationship. In diverging populations, as the location and degree of identity at potential crossover sites drifts, it becomes less and less possible to perform a successful meiosis, even if fertilisation produces a viable organism prior to that.
Allan Miller,
Good point, agreed. Not bad for a statistician, I might add.
Is there a reason for it or is it just a say-so? Is there something in that combination that makes it lethal or is this all under the umbrella of “let’s suppose”. Also, if genetic change occurs incrementally (individual by individual), then why would you say the *population* has fixed alternative genes?
Now, let’s suppose so and grant all that: Parts of population separate and they become distinct populations, first because of lack of interest/access to each other and eventually because of concrete failure to interbreed (“lethal combination” of genes). But earlier I read about a scenario where two plant species (cross-)bred yielding infertile hybrids, but somehow at some point they began yielding fertile hybrids, which was eventually labeled another species. So they merged or converged.
Given this, how is any of this determined by genes? It more looks like genes go along with the flow just like all the other organs with their shapes and forms and functions go along as “evolution” progresses (I’d say rather “circumstances change”). The variation is there, but it seems to have its limit, does it not? You can’t grow this or that part of your body as you wish – well, you can, but up to a limit. You can’t alter genes at will – well, you can, but it may turn out fatal. You can’t cross-breed whatever you like – well, you can, but a fertile result is rare, apparently determined by something. By what? Probably a combination of causes, genes being a factor, but how important a factor compared to the rest, and what are the other factors?
The claim of the evolutionary theory is that the variation has no limit, and cross-breeding (perhaps) has no effective barrier, over Very Long Time. The claim appears to be partially experimentally redeemed in the lower orders of nature (insects and plants), but it’s straightforward nonsense insofar as higher animals are concerned. So it’s very important to figure out what genes do, how they operate, what function they have for organisms, bearing in mind that just like any other organ may have different forms and functions in different species, so do genes.
Erik,
So it seems that you do indeed deny speciation has occurred. It’s interesting that biologists claim it has and you claim it has not. On what basis should I accept your viewpoint over theirs, when after all they have defined species and speciation in the first place?
It’s not an assumption, it is an evidentially derived conclusion. The “causal link” justification for that conclusion is basically that organisms reproduce in large populations, that descendants of their ancestors inherit their traits, that those populations some times split in two or more, and that this process inexorably produces divergent genealogical relationships (due to the mechanisms of genetics and inheritance).
No, but statistics can be used to answer questions relating to it. Such as, how do we know whether two species share common descent?
The above mentioned facts, combined with statistics, is how we know. The process of reproduction and splitting inexorably predicts highly congruent nesting hiearchies if the species share common descent, so when we find such highly conrguent nesting hiearchies, that is evidence that they share common descent.
Actually it is a genetics question. We are talking about inferring common descent using DNA sequences, so genetics has to be a central part of the answer. Or at the very least, the observational fact that traits are passed on in some way from parents to offspring.
So you’re here asking, essentially, what is the mechanism that results in a reproductive barrier, right? If that is what you meant to ask, there are many different ways reproductive barriers can emerge.
As some population splits in two, for whatever reason (changes in local geological features has diverted the path of a large river, carving the range occupied by a terrestrial species population of prehistoric Bovidae in two). So there is no longer any interbreeding going on between these two subpopulations, which means geneflow between them has dropped to zero.
At this point it might technically still be possible for them to interbreed should members from both populations ever happen to meet and attempt copulation.
But assuming this doesn’t happen (or only happens extremely rarely), then the two populations will diverge at the genetic level with every new generation born, because mutations are stochastically accumulating (meaning it is almost always not the same mutations that happen in the two populations) in their respective genomes.
So what happens is they drift further and further apart genetically such that, eventually, they have become so different that the molecular mechanisms that are normally responsible for pairing up chromosomes during genetic recombination, can’t effectively recognize each other any more. In this case, a full reproductive barrier has evolved.
Another way it could happen is that the proteins that cover the outside of egg-cels, which sperm-cells use to recognize egg-cells as egg-cells, have mutated so much between the two populations, that they can no longer bind together and trigger cell-fusion.
Another way still is what Corneel described above. This is by no means exhaustive nor are these examples mentioned in this order for any reason. The two hypothetical examples I gave here probably take a lot longer than the example Corneel gave.
Mung,
You can build genealogical trees when you don’t know how people are related, by using this phylogenetic nonsense.
There has been multiple independent gene-losses in the different isolated lineages in Richard Lenski’s Long-Term Evolution Experiment with E coli. Some lineages have lost multiple genes to large deletions.
See for example:
Richard E. Lenski. Convergence and Divergence in a Long-Term Experiment with Bacteria.
Am Nat. 2017 Aug;190(S1):S57-S68. doi: 10.1086/691209.
In this paper we find this gem:
” For example, all 12 populations completely lost their ability to grow on another sugar, ribose, over the first 2,000 generations of the LTEE (Cooper et al. 2001). In this case, the parallel losses resulted from deletion mutations that were demonstrably beneficial in the glucose-based medium and, moreover, occurred spontaneously at an exceptionally high rate. The high mutation rate was caused by a transposable element adjacent to the ribose operon that transposed into the operon and then underwent homologous recombination, leading to a deletion. These losses were so consistent across the replicate populations as to generate convergent, not divergent, outcomes.”
From:
Barrick JE1, Yu DS, Yoon SH, Jeong H, Oh TK, Schneider D, Lenski RE, Kim JF.: Genome evolution and adaptation in a long-term experiment with Escherichia coli.
Nature. 2009 Oct 29;461(7268):1243-7. doi: 10.1038/nature08480.
I have highlighted some rather large deletions (losses) with green arrows in this figure: See this link if the image quality is bad.
It turned out that we don’t have biologists here. We have statisticians. They are good at calculating probabilities, but they can’t explain what the probabilities are about.
The questions that I have do not concern probabilities or similarities, statistically significant or less significant. They are about causal relations in the given subject matter.