Evolution caught in the act

Earth’s tiniest predators and prey show ancestral genes morphing over many generations. Researchers track how descendants’ DNA molecules differ from those of ancestors. Molecular-level evidence of evolution’s acts aren’t possible with large charismatic animals.

Darwin puzzled over how truly new features could evolve. Molecule-level analysis could tell him. If he returned to the 21st century, this is what he’d want to see first.

Darwin knew plenty of examples of animal traits gradually improving: fur gets thicker, a neck gets longer, eyes get keener. But how can a wholly new feature – bats’ echolocation sense, for instance – arise from ancestors who had none of it?  That’s what these researchers came very close to showing.  Darwin’s era was ignorant of genes and molecules.  He could only guess how evolution altered animals’ “design blueprints.”  

The prey is the rod-shaped E. coli bacterium. Its shell, woven of proteins of different shapes, encloses the creature’s DNA and its chemical machinery of life.

The predator is a virus.  It uses a hook-like protein (called “J”) to anchor (like cockleburs on a trouser leg) onto the particular shape of a molecule on the prey’s protein coat. It then slithers through a pore in the coat. Inside, it hijacks the bacterium’s cellular machinery to make countless copies of the virus until the bacterium bursts. 

Is it disappointing that creatures with zero charisma reveal evolution’s action? Absolutely! Even worse: they’re invisible to our naked eyes. Obviously, genes in drab ancestral peacocks would be more thrilling to watch morphing into DNA for the iridescent tail. But extinctions destroyed ancestral peacocks in past eons. Those genes are forever lost.

With these bacteria and viruses, the genes are here today, in laboratory flasks.

On day 1, researchers filled 96 flasks with sugar solution inhabited by mutant E. coli. The mutants’ coat proteins were like Teflon to the J hook. Viruses couldn’t grab them, and so couldn’t attack.  In each flask, researchers eye-droppered in a dose of viruses to begin an arms race with the mutant bacteria. Would the predators evolve new weapons to defeat Teflon resistance? Or would they go extinct?  

Predators and prey proliferated into millions within hours, turning each flask cloudy. The researchers then created Generation #2 for each flask.  96 new flasks of sugar water received an eye-dropper load of their predecessor’s teeming liquid. Daily, for 28 days, the scientists repeated this.  Then they examined the 96 populations of predators.

24 of them — 25% — had evolved a new J hook whose different shape could hook onto “Teflon” bacteria. (The other 75% failed.) The predators had truly evolved a novelty. Not a peacock’s tail, but a true novelty. Success had taken 12 days, on average.

How, exactly, had predator genes changed?

The answer was: never in the same ways. In fact, none of the 24 successful predator populations mutated identically to any of the other 24. The genes defeated bacterial “Teflon” in 24 different ways.

So, was there any genetic pattern in successful predator mutants? Yes, there was some regularity. Four mutations were present in all 24 successes:

  • Two of them were identical: the same molecular change at the same location in the predator genome.
  • The other two mutations weren’t identical. But they did lie in the regions of genes that built J hooks. Nearby, it seemed, was close enough for anti-Teflon success.

But the the most interesting part of the novel J hook’s evolution was this. A predator had to possess all four mutations, but they didn’t arise simultaneously in one lucky generation. Instead, they accumulated and survived over multiple generations, despite the fact that  none of #1, 2, and 3 could defeat the Teflon, nor could any combination of them. Why (the researchers asked) would natural selection preserve those trivial mutations for generations until #4’s arrival would finally enable the lucky descendant to defeat the Teflon?

Darwin’s had guessed that novelties probably arise by co-opting an existing capability for a new purpose. That’s what these researchers supposed too: “presumably” (they wrote) mutations #1, 2 and 3 altered the J hook’s shape in ways that improved (somehow) its anchoring on normal prey. That would be a reason for preservation.

What those presumed improvements were, researchers couldn’t tell. But they had a surmise. They knew that small numbers of non-Teflon E. coli lurked among the Teflon ones in the 96 populations. Perhaps (they surmised), mutations #1, 2 and 3 allowed predators better to eke out survival for a few generations by attacking the small numbers of non-Teflon bacteria. Then, mutation #4’s arrival empowered them to conquer the copious Teflon bacteria infesting their flasks. But what the presumed improvement actually was, they could not detect.

What phenomenon in nature?

Evolution generates offspring that differ from ancestors.

What this discovery shows.

In one rapidly evolving creature….

  • Gene by gene causes of trivial changes over generations, that….
  • were followed by one more mutation that….
  • gave descendants a new capacity that no ancestor had. 

What was known before?

Other examples, but not with molecule by molecule demonstration.

What remains unknown?

Are molecule-by-molecule proofs possible with more interesting animals, like bats, peacocks, Emperor penguins, or even humans? Evolution in these roiling flasks of microscopic life seemed to be “just one damn thing after another” (as was said of human history by a prominent and cynical historian). Some underlying regularity would be more aesthetically pleasing.

J. Meyer et al., Repeatability and Contingency in the Evolution of a Key Innovation in Phage Lambda, 335 Science, 428-432, 27 January 2012 



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