Paul Nelson: Testing for Common Descent (Signal + Noise?)


(Timothy Horton) #60

Please clarify. Do your mean

  1. What series of observations if made in the last 100 years would have falsified the idea of UCD?


  1. What new observations made now would falsify the idea of UCD given the huge amount of positive evidence we already have for it?

(Paul A Nelson) #61

My arguments in this thread, as you’ll see from my omnibus reply, do not involve design. The entire time I was a student at the University of Chicago (1985-1997), I was not allowed to invoke design in my explanations, or in my dissertation.

One learns to probe assumptions in evolutionary theory from within evolutionary theory, which is what I’m doing here.


Would you agree that statistical tests (e.g. Paired T-test, ANOVA, regression) are a vital part of testing hypotheses?

(John Mercer) #63

Temin/Baltimore for reverse transcriptase, Cech and Steitz (separately) for ribozymes, Prusiner for prions.

(John Mercer) #64

I second Art’s. The discovery of an organism lacking the ribozyme peptidyl transferase certainly would make me question the hypothesis. This doesn’t preclude it using proteins, as despite your claim, there are other ways to catalyze peptide bonds.

(John Mercer) #65

I didn’t claim that you were arguing from design. I’m simply pointing out your labeling. Thanks for acknowledging that fact. It’s very important!

(Paul A Nelson) #66

Either – it doesn’t matter. By “counterfactual,” I mean only that we can describe observations, not yet made, which, if real, would cast serious doubt on UCD. Variant genetic codes were once such a counterfactual, until they were observed, and UCD was flexed to accommodate them.

I’ll give some examples later, from the current literature, where evolutionary biologists have argued that existing (real) observations are incompatible with UCD. Again, my interest turns on the logical structure of these arguments.

(S. Joshua Swamidass) #67

I can’t speak for others, but I do not have a desire to protect UCD, nor do I think it is nearly as important as other things, such as the common descent of man. The much more salient question is whether or not humans and apes share common ancestry. I’m not “committed” to the common descent of man, but merely feel it is critical to be honest about it.

(Blogging Graduate Student) #69

I don’t think reverse transcriptase could be considered “modifications to the axiom”, since the “axiom” (the central dogma, per Crick) originally accommodated reverse transcription in the first place. Likewise ribozymes (RNA -> RNA). Prions don’t strictly modify the central dogma since they don’t transfer sequence information.

Dan Graur drives these points home here (and in several other blog posts):

(John Mercer) #72

Interesting. Well, in my defense, I didn’t cite Crick. :sunglasses: Moreover, Crick said that RNA may be copied into DNA, while Baltimore and Temin showed that it actually was.

Finally, Crick’s stipulation of primary sequence information was made before anyone knew much about structure. Prions conferring infectivity on their normal counterparts definitely counts as information.

(George) #73


Most scientists handle this question poorly… out of inexperience with the notion i feel. I have answered this in a much older thread.

One or even a few findings like that would simply be considered an anomaly… much like the sometimes mysterious results physicists get in their atom smashing tests.

To truly overturn the Evolutionary model we would need a robust PATTERN of such anomalies (5 here, 10 on the other side of the world, and another 8 or so in a different ecosystem.

And then, it would have to be shown that Creationism AND A FLOOD somehow answers the riddle of those patterns better than evolutionary theories.

We are all still waiting for the first ONE incidence of any such pattern!

(Arthur Hunt) #74

Actually, Paul’s focus on the ribosome and not just rRNA is useful. If I am reading Paul correctly, his idea is that, in order to validate the notion that all rRNA-based life shares a common ancestry, there should be hypothetical scenarios or outcomes that would contradict the conclusion of common ancestry. “Foxoids” (which, just to be playful, could have been found around the newest lavabeds in Hawaii) are one such example – these cells plainly are devoid, not just of rRNA, but also of any hint of ribosomes. As I state above, these would refute the proposition that all life may share a common ancestry.

But what about rRNA and ribosomes? If one were to discover a ribosome variant in which the catalytic RNA core had been replaced with protein, would we conclude that such organisms do not share a common ancestry with rRNA-based life? (This possibility is an extension, perhaps an extreme one, of the finding that some mitochondrial ribosomes in fact have proteins that mimic, and replace, some structural domains of the rRNA. Not the peptidyl transferase, but other domains.) I would say, probably not. In this case, it would be the ribosome, the entire unit with structural features that include RNA and protein, that would argue for common ancestry.

We can extend these scenarios and ask – what about ribosomes (or ribosome-like organelles) that are devoid of RNA, in which all of the important parts of the rRNA have been replaced with protein structure mimics? I believe that, depending on the specifics, such an outcome could indeed call into question a deep shared ancestry with rRNA-based life. At the very least, the two opposing hypotheses would each merit serious consideration and experimental attention. (These would be fun experiments to do.)

Then there are yet other variations – for example, hypothetical enzymes that make protein without the mRNA-tRNA decoding system (that, incidentally, is an integral part of the rRNA system). The farther away we get from the ribosome, the stronger would be the conclusion that these organisms do not share a common ancestry with rRNA-based life.


I doubt that having two or three origins of life early in Earth’s history would do much to change the debate. At the very least, you would still have all eukaryotes, from protists to humans, sharing a common ancestor. I don’t see how that would be palatable to those who argue against evolution and common descent. In my judgement, the vast majority of people who argue against evolution and common descent can’t accept common ancestry between humans and other primates. Obviously, variations in genetic code don’t exist among primates, so why focus on that argument? The common ancestry they are really arguing about is much narrower than major divisions in groups of relatively simple organisms.


It may be worth mentioning that Darwin did not propose universal common descent. In fact, he was very open to multiple origins of life:

The reason that UCD is the scientific consensus is because of the evidence, not because the theory of evolution requires it. If there was evidence for multiple origins of life scientists would be absolutely fascinated by the findings.

(Timothy Horton) #79

OK then, go back to my previous example. AIG’s crack genetics lab manages to produce indisputable evidence Biblical “kinds” are a real category and that there exists a genetic barrier which makes it impossible (not just improbable) one “kind” can ever evolve into a different “kind”. They publish the results in Nature. Mainstream science looks at the data and goes “DOH! How in the world did we miss that?” and accepts the results.

That would kill UCD pretty dead, don’t you agree?

(Paul A Nelson) #80

Thanks to everyone who contributed to this discussion. Given its length, my reply will have to be divided into a few parts. What follows is part 1.

Preliminary note to T. aq. Your question about statistical methods raises important but complicated issues that require a separate thread, which I hope to begin in the next couple of days.

So who was the mystery philosopher of evolutionary theory, what did he say about the Precambrian rabbit test, and why does it matter anyway?

Elliott Sober of the University of Wisconsin. Here’s what he (and his co-author Mehmet Elgin) said, in context:

Evolutionary biologist John Maynard Smith (1986, 5) says that “the theory of evolution is not falsifiable in the sense required by Popper.” He says that the theory is a “logical deduction” and that Popper is demanding something more—that “a scientific theory must say something about the world, and not merely about logical necessity.” Maynard Smith goes on to say that “Darwinism as a testable scientific theory can take various forms. I will give it first in the form in which Darwin himself proposed it, and then in a ‘neo-Darwinist’ form in which most biologists hold it today.” Maynard Smith then says that the hypothesis of common ancestry is “clearly falsifiable . . . as a single fossil rabbit in Cambrian rocks would be sufficient.” This is a double mistake. The discovery that Maynard Smith describes would require an important reworking of when various taxa first appeared and how different taxa are genealogically related, but neither of these changes shows that the hypothesis of common ancestry is false. (emphasis added)

Complete text available here:

One could go many directions from a point like this. Maybe Popperian falsificationism is the wrong philosophy of science to adopt (as Sean Carroll has been saying lately), or maybe Maynard Smith, like the many other evolutionary biologists who have cited the Precambrian mammal test, was just confused (or maybe both). I want to go in a different direction, however. Popper and Maynard Smith aren’t my main interest.

Uncertainty about how to test universal common descent (UCD) persists 159 years after Darwin introduced the hypothesis. Ask a garden-variety evolutionary biologist about how he would know if UCD were false, and odds are, he’ll give some variant of the Precambrian rabbit test. But Sober thinks the test is a mistake, as do many of the people contributing to this thread. Why?

Until recently (see parts 2 and 3 of my reply), almost any biologist of repute would have said that UCD is a fact, and we don’t test facts; we take them as our unquestioned starting points in building theories. Within the ID research community, there’s significant debate about this, because some ID advocates, such as Mike Behe and Michael Denton, accept UCD, whereas others (e.g., Jonathan Wells, Doug Axe) are skeptics; others, such as Ann Gauger, can make a case on either side and remain undecided.

For several years, Discovery Institute has run a summer natural sciences seminar for students from around the world, to discuss the main issues of ID. My teaching responsibilities in the seminar include evo-devo and UCD (for and against). I found that, every July, a sizable percentage of my students accepted UCD, or found its factual status as plausible as any possible challenge to that status.

Here’s the sort of dialogue I’ve had with these students:

Student: We know that UCD is true because the genetic code is universal.

Me: The genetic code is not universal (

Student: These are minor exceptions. The genetic code is near-universal.

Me: “Near-universal” is a nonsense phrase, like “near-pregnant,” or “the number six is near-odd – on a good day it’s almost seven.”

Student: You know what I mean. The variant codes are not different enough from the universal code to qualify as inconsistent with UCD.

Me: So what variant code would be different enough to qualify?

Student: A code that could not have evolved from the universal code present in LUCA.

Me: Your answer entails that you know that the variant codes in the NCBI collection evolved from the universal code, and thus, how they evolved.

Student: I don’t know how those codes evolved, personally, but I’m sure someone does, because the biological community accepts UCD as fact.

Me: We can discuss the proposed hypotheses of code evolution later. They all have problems. But isn’t the real issue that UCD doesn’t predict variant codes? Hence, the empirical confirmation of UCD by the universality of the code, 1966 to 1985, was illusory, because UCD is equally well confirmed by the non-universality of the code, 1985 to 2018.

Student: UCD is not a predictive theory, at least not in the way you want. It’s an explanatory framework. And UCD doesn’t need confirmation any more, because everything we know in biology supports it.

Me: (sigh – thinking, what the hell is an explanatory framework?)

I realized that, to brings students face-to-face with the shortcomings of this “explanatory framework but not predictive” take on UCD, I would need to show them just how little UCD actually told them about the biological world, if they didn’t already know the answer from some other source.

So I devised a handout entitled "Phylogenetic Exercises," based on a simple device.

Take any biological character thought to be shared by two or more species, or any published phylogeny, and mask a portion of the character or character state distributions at the terminal taxa. Then ask someone to predict what characters or character states they should find on those masked branches, using only the phylogeny in question (i.e., no cheating by looking at PubMed or googling the answer).

Josh Swamidass has tried his hand at these exercises. I’ll send them to anyone who is interested (contact me at

While I need to re-design the phylogenetic exercises for a much larger sample, and need the help of a good statistician with other aspects of the experimental design, from casual inspection of the results so far, the answers look to be no better than random.

In other words, if one does not know the outcome already, UCD – whether in its fully universal form, from LUCA, or for some clade within the Tree of Life, such as the vertebrates – gives no guidance. One may as well toss a coin or roll a die.

Turns out this result has been known for a long time:

A given tree hypothesis is logically congruent with any specific observable evidence of character state distribution. In other words, a given tree, in combination with decent with modification as background knowledge, does not prohibit any specific character state distribution pattern (Farris, 1983; Sober, 1983). As there is no deductive link between any tree hypothesis and any specific character state distribution there exists no direct empirical test of hypotheses of monophyly (i.e., clades) sensu Popper (Sober, 1988; Rieppel, 2003)—one cannot think of any observation, which, in case it would represent a true statement, would allow to conclude the falsity of a clade or a given cladogram through modus tollens. (emphasis added)

From here:

Here endeth part 1. Thanks again to everyone who commented. More to follow, gotta do my day job or Discovery Institute will come looking for me with a Doberman.

Nelson's Test of Common Descent Comprehension

For the purposes of this thread, universal common descent isn’t even the question. The real question is if divergent species, like a human and a trout, share a common ancestor. Casting doubt on UCD does not cast doubt on CD.

Let’s say there was 3 origins of life early in Earth’s history. These gave rise to 3 domains of prokaryotes. From those three domains evolved the biodiversity we see today. Does this cast doubt on the claim that humans and other vertebrates share a common ancestor? No.

So what exactly are you arguing against?

(Paul A Nelson) #82

Surrender UCD, and the Tree of Life begins to come apart from its base. Molecular characters which, under UCD, indicate monophyly, no longer carry the signal of history (shared ancestry) and it becomes impossible to stop the fracturing as one climbs up into the branches of the tree (e.g., your example of trout and humans).

More about this consequence in parts 2 and 3.


All it does is create multiple trees. Instead of 1 tree we have 3. The species in each tree are still related to each other by common descent.

That is false. If there are characters that evidence independent ancestry that doesn’t make the evidence for shared ancestry go away.

(T J Runyon) #84

I feel like this is nonsense. “Near Pregnant” or “the number six is near odd” is nothing like saying “almost all” which is what near-universal means here.