Now and then, I hear a critic attempt to spin front-loading evolution as some form of back-peddling or moving the goalposts. Unfortunately for such critics, the internet has a memory and I have shown before, I have been raising the hypothesis of front-loading since the early 2000s. Here’s something I wrote on a forum known as Brainstorms back on May 7, 2002:
Yes, an imperfect replicator will necessarily evolve. But this does not mean unicellular organisms will necessarily evolve into a multicellular organism. In fact, a planet-full of unicellular organisms could very well undergo billions and billions of years of darwinian evolution without ever evolving a multicellular organism. My perspective explores the possibility that unicellular organisms were designed in such a way that the evolution of multicellular organisms was made more likely.
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It seems to me that an effective front-loading strategy would have to employ things like preadaptation, cooption, and buried design. The alternative is to directly design all the genes needed far in the future and deposit them in the present. The two main design problems come with storing all this information and maintaining it until it is used. Preadaptation, cooption, and buried design are solutions to these design problems.
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I already explained that the outcome of FLE is the thing in question. But logically, the best place to start, after positing that the original life forms were unicellular organisms seeded on this planet, would be to investigate whether such cells were front-loaded to evolve into multicellular organisms. So I’ll put that hypothesis on the table.
Six years later and it appears that my original hypothesis is much, much stronger. Why? Simply read all the blog entries marked ‘front-loading.’ And that was just from this year with a lot more to come.
We’ve seen that the neurotransmitters acetylcholine and epinephrine were in existence long before the evolution of the nervous system. So I decided to dig a little deeper.
Our star for the day will be the humble paramecium. You may remember looking at these little critters in a high school biology course, but if not, you can watch them in the video below.
Perhaps it would help to pause and define a kluge (often spelled as kludge). Let me quote from Gary Marcus, who defines it as follows:
A kluge is a clumsy or inelegant solution to a problem that gets the job done, but not necessarily in the best way possible.
Good definition. And note the vital ingredient as far as the blind watchmaker is concerned – “gets the job done.” That is all that is needed. As long as a solution gets the job done (and getting the job done is simply about reproductive success), it gets selected. The blind watchmaker is blind because it cannot see if a solution is clumsy, inelegant or entails an immediate payoff at a future cost; it only sees whether or the not the immediate job is done. This is why we expect kluges from the blind watchmaker.
I don’t mean to keep going on and on about this topic, but the story is writing itself. We’ve seen that many preadaptations for the evolution of neurons were in place. Calcium toolkit for secretion of neurotransmitters? Check. Post-synaptic scaffold? Check. Circuitry for neurogenesis? Check. But what about the neurotransmitters themselves?
Now, in principle, just about any molecule could serve as a neurotransmitter since it functions as a signal. You simply need something that specifically binds to a receptor that in turn triggers the opening of an ion channel. In fact, some amino acids, like glutamate, can moonlight as neurotransmitters.
Nevertheless, I decided to check up on two important neurotransmitters – acetylcholine and epinephrine.
Let’s now dig a little deeper into the rabbit hole where sponges contain significant chunks of the developmental circuitry needed for neuron formation. Stick with me and I’ll show ya something pretty cool (albeit with some over-simplification).
What is truly neat about this study is that the researchers did not merely find gene sequences, they actually tested the function of one of the key sponge genes (AmqbHLH1) in a deeply significant manner.
First, they noted, “Phylogenetic analysis suggests that AmqbHLH1 is homologous to all the atonal-related bHLH genes found in bilaterians, including the proneural genes atonal and neurogenin.Accordingly, the bHLH domain of AmqbHLH1 shows a mixture of conserved amino acid residues observed in the bHLHs encoded by the different atonal-related bHLH genes but only a limited similarity to any one gene in particular. The atonal genes are important proneural genes in Drosophila, and the neurogenin genes are important proneural genes in vertebrates.”
In other words, atonal is the fruit fly version of the sponge gene and neurogenin is the vertebrate version of the sponge gene. And when we look at the sequence of the sponge gene, it is a mosaic of the fly and frog gene.
For the past several years, I have been focused on how one might facilitate the evolution of metazoa. But because of recent scientific discoveries, I should pause and comment on an old topic - the bacterial flagellum.
Five years ago, I wrote an essay that raised many questions and expressed skepticism about Nick Matzke’s hypothesis of homology between the bacterial flagellum and the F ATPase. At the time I wrote this, the skepticism was justified. But since then, new data have come in that have served to significantly strengthen Matzke’s hypothesis and undercut my skepticism.
September 30th, 2008 by 
Mike Gene 
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