This is a quick rebuttal of the thesis explained by David Dobbs in his recent “Die, selfish gene, die” Aeon Magazine article [Edit: 14/12/2013 now archived here]. It is a well written, well documented and quite long piece that tries to explain why we should consider the “selfish gene” metaphor outdated and substitute it with more “correct” ideas. The article shows two, very rare, and highly appreciated qualities: the author is very careful in pointing to all his sources (he had plenty) and also did manage to get Richard Dawkin’s opinion directly. I want to point this out because both things are rare, and essential for good science communication. The rest of this post will be highly critical of the article contents, so I would like to make sure the reader remembers this short initial praise: it is deserved and nothing of what I’ll say below invalidates it.

Having said this, the content is so wrong that I actually had to force myself to read it all, it was intellectually painful, but I’ve managed.

Dobbs cites Gregory Wray, a biologist at Duke University in North Carolina:

‘Different groups of animals succeed for different reasons,’ says Wray. ‘Primates, including humans, have succeeded because they’re especially flexible. You could even say flexibility is the essence of being a primate.’

and then adds:

According to Wray, West-Eberhard and many others, this recognition of gene expression’s power requires that we rethink how we view genes and evolution. For a century, the primary account of evolution has emphasised the gene’s role as architect: a gene creates a trait that either proves advantageous or not, and is thus selected for, changing a species for the better, or not. Thus, a genetic blueprint creates traits and drives evolution. […] But a number of biologists argue that we need to replace this gene-centric view with one that more heavily emphasises the role of gene expression — that we need to see the gene less as an architect and more as a member of a collaborative remodelling and maintenance crew.

I can live with all this, as long as one notices that the ability to dramatically change the gene expression patterns is a ‘trait’ in its own right, that this ability is inherited like any other trait, and that (unless a different carrier of inheritable information is identified) the information that makes this trait possible is stored in the subject’s DNA (somewhere, somehow, the details are irrelevant for now).

Dobbs also cites Michael Eisen, an evolutionary biologist who researches fruit flies at the University of California, Berkeley:

‘It’s not that genes don’t sometimes drive evolutionary change. It’s that this mutational model — a gene changes, therefore the organism changes — is just one way to get the job done. Other ways may actually do more.’

and then adds:

Like what other ways?

There are several, but one called genetic accommodation is, according to West-Eberhard, particularly powerful and overlooked.

West-Eberhard is Mary Jane West-Eberhard, a wasp researcher at the Smithsonian Tropical Research Institute in Costa Rica who appears to have inspired most of the article. In fact, this is where the whole argument derails beyond repair.

The first warning sign:

[genetic accommodation] takes a moment to explain. But bear with me a moment, and you’ll understand how you, dear reader, could evolve into a fast and deadly predator.

What? I can personally evolve into something else? I can change my own genetic blueprint, in a meaningful way during my life (leaving alone notable exceptions such as antibody recombination)? Seriously? Wow, I’d better read on! (In fact, by this point I was already forcing myself to keep reading)

For example, suppose you’re a predator. You live with others of your ilk in dense forest. Your kind hunts by stealth: you hide among trees, then jump out and snag your meat. You needn’t be fast, just quick and sneaky. Then a big event — maybe a forest fire, or a plague that kills all your normal prey — forces you into a new environment. This new place is more open, which nixes your jump-and-grab tactic, but it contains plump, juicy animals, the slowest of which you can outrun if you sprint hard. You start running down these critters. As you do, certain genes ramp up expression to build more muscle and fire the muscles more quickly. You get faster. You’re becoming a different animal. You mate with another fast hunter, and your kids, hunting with you from early on, soon run faster than you ever did. Via gene expression, they develop leaner torsos and more muscular, powerful legs. By the time your grandchildren show up, they seem almost like different animals: stronger legs, leaner torsos, and they run way faster than you ever did. And all this has happened without taking on any new genes. Then a mutation occurs in one grandkid. This mutation happens to create stronger, faster muscle fibres. This grandchild of yours can naturally and easily run faster than her fastest siblings and cousins. She flies. Her children inherit the gene, and because their speed wows their mating prospects, they mate early and often, and bear lots of kids. Through the generations, this sprinter’s gene thus spreads through the population. Now the thing is complete. Your descendants have a new gene that helps secure the adaptive trait you originally developed through gene expression alone. But the new gene didn’t create the new trait. It just made it easier to keep a trait that a change in the environment made valuable. The gene didn’t drive the train; it merely hopped aboard.

Right, I’d better study more English, ’cause I thought that fast and quick were synonyms, but I’ll leave semantics aside and dive into the core argument.

The citation above is the key argument here. We should remove genes from the centre stage of our understanding of evolution and replace it with something else, presumably the environment-dependent variability of gene expression, or maybe the concept of genetic accommodation itself. We may do that, but it is crystal clear that the variability of gene expression is the result of some more genes, their interaction with non-encoding parts of the DNA sequence (those little things that we molecular biologists call promoters) and all the associated machinery.

What this means is that the variability of genetic expression is a genetic trait, making the story above incomplete: it lacks a crucial detail about what happened before. The genetic-expression variability that allows our predator to “train” and get faster exists as the direct result of natural selection itself, and the trait that was positively selected is the ability to change the expression patter so to build more muscle. We know this because genetic expression is demonstrably regulated by proteins that interact with specific DNA sequences (as well as other systems that act further down across the line, changing what happens to messenger RNA and so forth). In other words, it all boils down to other genes (the ones that encode for the regulators) or DNA sequences (the promoters and similar trickery). So no, we don’t need to put aside the “selfish gene” idea, we may acknowledge that things get fantastically complex in almost all cases (very rarely one gene encodes for one and only one phenotype), that most biologically interesting phenomena happen because of the interplay of genetic networks (where one up-regulates the expression of some, down-regulates some others, and all genes involved may have some other effect elsewhere), and that saying “one trait corresponds to one gene” is usually wrong.

But that is all. Claiming that we need new evolutionary concepts to replace the faulty idea of the selfish gene is just downright wrong. What we do need to understand and model in new and more reliable ways is how a genome entirely made up of selfish genes (and other selfish non-coding sequences) can evolve to create monstrously complex networks that allow the astonishing adaptability of human bodies. The challenge is to see how, why and when “selfish”* elements associate and “collaborate” in ever more complex ways (generating the variability that is impossible to pin down to a single gene). I will not discuss this here: there are lots of things we understand about this mechanism, and lots more that are being researched intensely, but the challenge is about how “selfish” elements invariably produce “collaborative” networks in which each single element depends on all the others. This is important, and very interesting, because it happens on many levels: for example, in a previous post, I have hinted about this kind of problem in the domain of human collaboration (see the “Edge” link).

But for now, I’ll finish it here: Dobbs claims, with the crucial support of West-Eberhard that:

By the time you’ve finished his book, or well before that, Dawkins has made of the tiny gene — this replicator, this strip of chemicals little more than an abstraction — a huge, relentlessly turning gearwheel of steel, its teeth driving smaller cogs to make all of life happen. It’s a gorgeous argument. Along with its beauty and other advantageous traits, it is amenable to maths and, at its core, wonderfully simple. Unfortunately, say Wray, West-Eberhard and others, it’s wrong.

And that’s pure nonsense, bad reasoning and misinformation.

*Note the quotation marks: “selfish” and “collaborate” are used here as metaphors. There are very little reasons to believe that genes are conscious, so they can’t be “selfish” or “collaborative” as humans would.

PS: (added on 14/12/2013) David Dobbs has published a new version of his article, I’ve responded to it here.