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Richard Dawkins’s Unlikely Nemesis 

Photo: Copyright holder: Denis Noble ("I certify that I own the copyright to this photograph."), Copyrighted free use, via Wikimedia Commons.

Back in 2016, The Guardian ran a glowing piece for the 40th anniversary of the publication of Richard Dawkins’s influential book The Selfish Gene, which argued that organisms (like humans) are merely the vehicles that genes use to survive and propagate themselves. The author of the piece, evolutionary biologist Adam Rutherford, wrote that the book’s fame would last forever, for “as long as we study life, it will be read.” 

Yet even in 2016, Dawkins’s selfish gene model had begun to come under attack from other scientists. Since then, the cracks in the theory have grown. 

Leading the charge against the model is — of all people — Richard Dawkins’s own doctoral examiner at Oxford, the renowned physiologist Denis Noble (who at 87 is as old as you might imagine he must be, to be Dawkins’s examiner — yet still enjoys ballroom dancing).

In June 2022, the two scientists clashed in a lively debate (surprisingly lively, you might say) at the HowTheLightGetsIn music and philosophy festival in England. Despite his fame as a debater, Dawkins did not seem to be able to hold his own against the older professor. Since then, Noble has (rather endearingly) made it an annual tradition to trash Dawkins’s hypothesis at that festival: in May 2023 he gave a lecture about why the selfish gene model is wrong, and a few days ago, on May 25, he returned to the festival for the same reason. 

The new evidence Noble highlights is truly fascinating. Since many readers may not have been following the feud over the last couple years, I thought it would be worthwhile to give a brief account of the conflict here.

Intelligent Cells

Noble’s thesis is quite simple: Dawkins’s hypothesis has been disproved, and should be discarded. The science has shown that organisms use genes to make the molecules necessary for reproduction, not the other way around. 

In the debate, Dawkins summarizes Noble’s view rather dramatically:

Dawkins: In a way, he’s implying that when this cell needs to make a protein it goes into the nucleus and consults the library, which is the genome, and takes down the volume relevant to the enzyme that’s needed…

Noble: Absolutely! [Laughing]

Dawkins: …and, “This is the one we need. We need to make this protein. Let’s get the relevant gene out and use it.” That is Denis’s view. He’s nodding vigorously. 

Noble: Absolutely. [Laughing]

It’s no wonder Dawkins is opposed to this idea. It seems to reek of intelligent design — and not merely at the moment of origin of a species, but perhaps even at the moment of cellular replication. Yet if Dawkins’s strategy was to trap Noble in an absurd position, it didn’t work, because Noble goes on to back his view up with experimental evidence. 

Noble points out that if you put a genome in a petri dish and left it for ten thousand years, you would not get an organism. Dawkins replies that this is true — however…

Dawkins: However, the information, it could be preserved on paper. You could actually write it down in a book, you could carve the A, T, C, and G codons in granite and keep it for ten thousand years, and then in ten thousand years type it into a sequencing machine (which we already have) and it would recreate an identical twin of Denis Noble.

Noble: I don’t think it would.

Dawkins [surprised]: You don’t think it would?

Noble: No. 

Dawkins: Why not?

Noble: Well, it would need an egg cell.

Dawkins: Oh, of course it would!

Noble: [laughing] Yes! Yes, I think we need the egg cell! 

Dawkins: In ten thousand years, they will have the technology to take an egg cell.

Noble: Oh, I see. I now, therefore, need to follow up on a different issue then — if I may — Richard, yes, because, you see, what you would need to be is a good self-replicator. And you won’t be surprised that I disagree with you on self-replication, because I think that’s a central feature. Because I think without the self-replicator, I’m not quite sure that I understand what the selfish gene idea really means. Now let me just explain briefly why it can’t be a self-replicator…

Gene self-replication tends to have one error in 10,000, Noble says. However, when the cell divides, you find that instead of being accurate to one in 10,000, it is accurate to one in 10,000,000,000! That is because the cell actually proofreads the genome after replication. 

Noble: That’s rather like a proofreader of ten thousand books going through ten thousand books and making sure there’s not a single error in the whole ten thousand books. How is that achieved? It’s utterly amazing, it’s achieved by the living cell! Because what then happens, as the problem of the breakages, as we might call them, in the DNA formation from the double helix when it’s unwound, what then happens is a whole army of enzymes go in and literally proofread the mistakes! That’s why I say you’d have to put my genome in 10,000 years hence into a living cell to do it. Now the question is, which living cell?

Lamarckian Tube Trains 

In response to this mind-boggling piece of information, Dawkins basically just rehashes the selfish gene hypothesis: Information flow goes only one way; from the genes to organism. Changes in genes, then, have to be what ultimately determines the nature of the organism. Traits that help the gene be passed on are the traits that are favored by natural selection. The genes are the reason the organism exists, not vice versa.

Noble replies that Dawkins has not answered his point. He explains recent discoveries about how the cell proofreads the DNA, from the work of two of his colleagues:

What they’ve shown is best described by imagining, first of all, that a single nucleotide is about the size of my fist. And it’s situated in the nucleus, so let’s put that in the center of the cell. If we did that, on that scale, the surface membrane of that cell would be way up in Scotland. How on earth can it be that a signal through a receptor on the surface can influence the nucleus? And we now know how that can be done. What they both found, doing different experiments in different cells, was that calcium coming through protein channels in that surface membrane — using the same metaphor; way, way up there in Scotland — creates a calcium concentration in a small subspace underneath the membrane, and that high calcium triggers a chemical reaction that produces a messenger. And that messenger gets attached to some extremely important proteins in the cell. Those proteins are called tubulins. And the name suggests what they do — they form tubes. Literally, there are tube trains in cells. And I’m not joking, because what happens is those tubulins run all the way through from one edge of the cell to another. They have little motors on them, little molecular motors, and they can attach a messenger molecule to that motor. And what then happens is phenomenal. They literally walk along the tubulin. It takes just a few seconds to go from that surface — imagine on this scale way up there in Scotland — to the nucleus. What does it do? In those experiments it changes the gene expression in the relevant genes that matter for that particular function. 

He goes on to say experiments have shown that these processes do not merely affect expression, but actually introduce genes into the germline.1

Noble: I’m sorry to say this because I know this is a dirty word amongst most evolutionary biologists, but — Lamarck is back! Very simple. 

Dawkins ultimately admits that if what Noble is saying is true, he would have to revise his theory. But he says, rather lamely, that he doubts it is true.

All told, it was surprising to see how badly Dawkins did in the debate, given his reputation as a debater, and given that he projects a much younger and more vigorous image than the venerable Noble. The best that can be said is that Dawkins was at least very courteous — he even asked Noble to sign his copy of Noble’s book at the end of the debate. 

Get with the Times!

Noble followed the debate with an interview (“Why Dawkins is wrong”). He said: 

…I don’t think the great majority of research biologists are any longer following that path, in the way in which he [Dawkins] laid it out. So I’m sorry to say I think the ground has shifted quite a long way. You see, in the debate we’ve just had… it seems to me that what that showed was that I don’t think people like Richard yet know that; that things really have moved on very rapidly. Did we know a few years ago that there could be tiny particles that could carry RNAs and DNAs to the germline? No, we didn’t. That’s within the last 20 years. So there is a shift here. It’s, in principle, of enormous proportions. And whether people are waking up to that in the public media, I rather doubt. But they really should, because it has big, big implications.

In his lecture at the same festival a year later, Noble says that the genetic code is not a code, like computer program, because there are no if/then pathways in it. Rather, it is like a template or music score, which has to be interpreted. He says that the selfish gene model has held back medicine, and, for that matter, that no aspect of society can have escaped the effect of the selfish gene myth. Yet the science has moved on, and Noble is not sure why textbooks still teach a model that has been debunked experimentally. 

Despite all this, Noble is a committed Darwinist. (At one point, the Dawkins/Noble debate broke down into an argument over whether Noble really gets to call himself a Darwinist!) 

Dawkins, at least seems to understand that you need a Darwinian model that clearly shows how complex systems can develop by unguided processes. Noble doesn’t seem to see the problem, but how do you get a system that can go to the “library,” take down the correct volume, and proofread it? It strains credulity. At any rate, Dawkins’s The Selfish Gene does not look nearly so immortal now as it might have in 2016. I’m curious to find out if the pieces written in 2026 for the 50th anniversary of the book will be different from those written for the 40th. Perhaps not; science moves quickly, but scientism can be very slow.

Notes

  1. The references for these studies are provided in the notes of the transcript of the debate: Ma, H., Groth, R. D., Cohen, S. M., Emery, J. F., Li, B., Hoedt, E., et al. (2014). γCaMKII shuttles Ca2+/ CaM to the nucleus to trigger CREB phosphorylation and gene expression. Cell, 159, 281–294. Kar, P., Mirams, G. R., Christian, H. C., & Parekh, A. B. (2016). Control of NFAT isoform activation and NFAT-dependent gene expression through two coincident and spatially segregated intracellular Ca2+ signals. Molecular Cell, 64, 746–759. Zhang Y, Zhang X, Shi J. et al. (2018). Dnmt2 mediates intergenerational transmission of paternally acquired metabolic disorders through sperm small non-coding RNAs. Nat. Cell Biol. 20, 535–540. https://doi.org/10.1038/s41556-018-0087-2