I won’t attempt to summarize Behe’s entire book nor our short review, as people can read those for themselves if they want. Instead, I hope to accomplish three things in this post and two more that will follow.
In this first post, I explain why Behe’s so-called “first rule of adaptive evolution” does not imply what he says it does about evolution writ large.
In the second post, I’ll discuss whether my long-term evolution experiment (the LTEE for short) does or doesn’t provide strong support for Behe’s position in that regard.
In my third post, I’ll explain why I think that Behe’s positions, taken as a whole, are scientifically untenable.
(numbers added)
Summing up, Behe is right that mutations that break or blunt a gene can be adaptive. And he’s right that, when such mutations are adaptive, they are easy to come by. But Behe is wrong when he implies these facts present a problem for evolutionary biology, because his thesis confuses frequencies over the short run with lasting impacts over the long haul of evolution.
Behe’s next sentence then asserts the power of the “de-evolutionary” process of gene degradation. This is an unjustifiable extrapolation, yet it is central to Behe’s latest book. (It’s not the sort of error I would expect from anyone who is deeply engaged in an earnest effort to understand evolutionary science and present it to the public.) Yes, natural selection sometimes increases the frequency of broken and degraded genes in populations. But when it comes to the power of natural selection, what is most frequent versus most important can be very different things. What is most important in evolution, and in many other contexts, depends on timescales and the cumulative magnitude of effects . As a familiar example, some rhinoviruses are the most frequent source of viral infections in our lives (hence the expression “common cold”), but infections by HIV or Ebola, while less common, are far more consequential.
Lenski publishes part one of a three part series explaining in more detail his take on Behe’s rule.
I would also like to make a prediction. Even though Tiltaalik has really nothing to do with this, when they review this they will mention Tracks from Poland and how it rules out Tiktaalik as a transitional (though they have been corrected on this a hundred times)
In the same vein, even if many more mutations destroy functions than produce new functions, the latter category has been far more consequential in the history of life.
How do you think he has supported the claim that the mutations that are bring new functions are random with respect to fitness?
I’m curious too. The nearest I can find is the following, and it’s not what @colewd suggests.
From the blog:
[…] (iii) even those degradative mutations that are not helpful on their own sometimes persist and occasionally serve as “stepping stones” on the path toward new functionality. This last scenario is unlikely in any particular instance, but given the prevalence of degrading mutations it may nonetheless be important in evolution. (This scenario does not fit neatly within the old-fashioned caricature of Darwinian evolution as only proceeding by strictly adaptive mutations, but it is certainly part of modern evolutionary theory.)
In the same vein, even if many more mutations destroy functions than produce new functions, the latter category has been far more consequential in the history of life.
They painted themselves into a corner here. We told them upfront that there was more coming and the science review was just a starting point. We encouraged them to engage with us to clarify.
Then came the self parody we just saw.
We had explained we would expand on all this from the beginning, but I wonder if they will try and ingore this. It isn’t fitting the narrative they are pushing.
Mutations are random . Mutations can be beneficial, neutral, or harmful for the organism, but mutations do not “try” to supply what the organism “needs.” … In this respect , mutations are random — whether a particular mutation happens or not is unrelated to how useful that mutation would be.
Bill, it would help to review your original claim:
To be fair, that might not be what you intended to say, because you aren’t very good at expressing yourself. But that claim above isn’t talking about all mutations, just mutations that bring new functions. Mutations that bring new functions are a chosen subset of all mutations, chosen because they bring new functions. And new functions, almost by definition of the term “function”, are likely to be beneficial. In short, one would expect mutations that bring new functions to be highly biased toward those that increase fitness.
This, however, has nothing to do with what biologists and the Berkeley web site actually say: that mutations, not just the carefully selected subset that bring new function, are random with respect to fitness. That is, mutations don’t happen because they would be helpful (or otherwise); they just happen. This is the import of the Luria-Delbruck replica plating experiments and of much subsequent investigation.