I am not sure it’s fair to call this one a just so story… but I am also not sure what is being described is evolution. Look at how Jerry coyne describes the process in his blog -
What’s remarkable about this configuration is that every bit of it, including the two proteins themselves and the promoter sequence, was cobbled together via translocations and duplications of DNA (this happens passively in the genome) until all the elements were in place. And the “functional” gene couldn’t function right up to the very end, when the promoter sequence moved to the right place to allow the protein-coding region to produce an RNA transcript. This entire series of steps was reconstructed by sequencing the DNA of relatives that don’t have functional AFGPs, so we could see the evolutionary order in which things were assembled, and where the functional bits originally came from.
He is describing a series several steps in a particular order which are supposed to have happened by accident without the help of even selection to give it any direction. He is essentially describing a miracle. Organisation without any reason or cause.
After these 6 events happen by “serendipity” or “Providence”, Jerry coyne claims the below-
Further, natural selection could now act on the functioning gene to make it more effective, simply by selecting for those genes that had even more duplications of the Thr-Ala-Ala segment, so we had a big protein of repeated units that could act as an antifreeze in fish blood (E—>F). (More repeats = better antifreeze protection.)
It’s a bit more complicated than this, but this is the essence of how the final protein came to be. And it’s not speculation, because all the bits can be found in other species or posited in ancestors, and so this reconstruction is fairly sound. Moreover, it involves processes known to operate in the DNA: the moving of bits around by translocation, duplication of sequences, etc. No divine intervention is required to do this, even though the protein isn’t functional until it’s put together with the secretory protein and the promoter.
On top for that the process needs to happen very fast so that mutations don’t mess up the work done in each step. Here is coyne’s explanation-
One might ask this reasonable question: “Well, if the nascent antifreeze protein is just sitting there and not doing anything before it becomes active, why isn’t it inactivated by mutations?” That’s a good question, and one answer is that the process took place reasonably quickly so that mutations (which are, after all, rare) didn’t have time to turn the dark blue protein core into gibberish. And once that core formed, duplication of the Thr-Ala-Ala would be rapid, promoted by natural selection because more repeats confer greater antifreeze activity.
And lastly, it’s not clear whether small concentrations (starting from one case?)of the “thr-Ala-Ala” are effective enough to be “selected” for their anti freeze properties.
All I will say is that I don’t have as much faith in serendipity and coincidence as Jerry does. And that somebody like James Shapiro would explain this entire scenario differently in a more plausible way… (not that I would agree with him ).