compensatory evolution

Bullaughey K 2013 Multidimensional adaptive evolution of a feed-forward network and the illusion of compensation. Evolution, in press.
doi:10.1111/j.1558-5646.2012.01735.x

  • the possibility for compensatory evolution results from epistasis
  • yet if epistasis is widespread, then it is also possible that the opposing substitutions are individually adaptive
  • I term this possibility an adaptive reversal
  • there are a number of a priori reasons why one might not expect adaptive reversals to be a common feature of regulatory evolution
  • the bulk of epistatic interactions may be among nucleotides involved in encoding a single biological function
  • epistasis may be common within a protein, where there may be many interacting residues
  • but less common between proteins, because interaction surfaces may be limited to a subset of domains and residue
  • epistasis in regulatory networks may be limited by the modularity characteristic of networks
  • in a multi-component, adaptively evolving system, adaptation may be an especially strong driver of epistatic changes in the genetic background, making the assumption of no epistasis less plausible
  • adaptive reversals may not be surprising when one considers the dizzying possibilities for arbitrary high-dimensional fitness landscapes
  • that adaptive reversals occur in a relatively low-dimensional, biologically plausible model for regulatory function, is important
  • focusing on a single trait at a time rather than the system in which it is embedded could mistakenly lead one to infer the trait to be evolving under stabilizing selection (via compensatory evolution), when it is actually one component of an adaptively evolving system
  • the substitutions of opposing functional effect may even be helpful in detecting adaptation, when combined with data from other coevolving traits
  • in the adaptive walk simulations, I accept or reject each mutation based on the fixation probability
  • successive substitutions are independent
  • this approach does not model certain population dynamics including the joint substitution of mutations or interference among simultaneously segregating mutations
  • these dynamics are likely to be of very minor importance here
  • by deliberately excluding them, I ensure that the substitutions comprising the adaptive reversal are indeed individually beneficial