Lovely paper. The bug we work on, Neisseria gonorrhoeae, has *hundreds* of genes that can phase-vary (stochastically switch on and off), to allow immune evasion and adaptation to different niches within and between hosts. 1/
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This new paper uses laboratory evolution to test the hypothesis that the sorts of selective regimes that many of us thought produced these systems, can indeed cause these systems to evolve. Terrific stuff. 2/2
Addendum: the underlying mechanism, appearance of tandem repeats of length multiples ≠3, which throw the reading frame in or out by insertion or deletion of repeats, is the same in N. gonorrhoeae and in the lab studies above. The proposed slipped-strand mispairing is also similar.
Ditto for gut symbionts. But I'd curious to quantify what the cost of this phenomenon is in the context of a highly competitive complex community vs. single species
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