Fast evolution of bacteria after a host shift

Ultrafast Evolution and Loss of CRISPRs Following a Host Shift in a Novel Wildlife Pathogen, Mycoplasma gallisepticum

By Delaney NF , Balenger S , Bonneaud C , Marx CJ , Hill GE , et al.

in PLoS Genet 8(2): e1002511. doi:10.1371/journal.pgen.1002511 (open access)

(See below for a note from one of the co-authors, Allen Rodrigo, Director of NESCent.)

Abstract:  Measureable rates of genome evolution are well documented in human pathogens but are less well understood in bacterial pathogens in the wild, particularly during and after host switches. Mycoplasma gallisepticum (MG) is a pathogenic bacterium that has evolved predominantly in poultry and recently jumped to wild house finches (Carpodacus mexicanus), a common North American songbird. For the first time we characterize the genome and measure rates of genome evolution in House Finch isolates of MG, as well as in poultry outgroups. Using whole-genome sequences of 12 House Finch isolates across a 13-year serial sample and an additional four newly sequenced poultry strains, we estimate a nucleotide diversity in House Finch isolates of only ~2% of ancestral poultry strains and a nucleotide substitution rate of 0.8−1.2×10⁻⁵ per site per year both in poultry and in House Finches, an exceptionally fast rate rivaling some of the highest estimates reported thus far for bacteria. We also found high diversity and complete turnover of CRISPR arrays in poultry MG strains prior to the switch to the House Finch host, but after the invasion of House Finches there is progressive loss of CRISPR repeat diversity, and recruitment of novel CRISPR repeats ceases. Recent (2007) House Finch MG strains retain only ~50% of the CRISPR repertoire founding (1994–95) strains and have lost the CRISPR–associated genes required for CRISPR function. Our results suggest that genome evolution in bacterial pathogens of wild birds can be extremely rapid and in this case is accompanied by apparent functional loss of CRISPRs.

The note below is from one of the co-authors, Allen Rodrigo, Director of NESCent

What I find really interesting is the loss of the phage defense CRISPR mechanism.  It turns out there is evidence that a similar thing happens when HIV moves from one individual to another – when it enters a new (recipient) host, it loses the epitopes that allowed the virus to escape evasion in the original (donor) host, and acquires a new set of substitutions.  We think this happens (and there is some evidence for this) because epitopes that confer immune protection are costly in terms of reproduction.  So, the mycoplasma-house finch story is part of a larger story about the dynamics of transmission, either across hosts or across species.  It raises another really interesting question: if this phenomenon is generally true (i.e., that immune-escape variants are less reproductively fit, and that successful transmission leads to the loss of previously acquired substitutions), it may explain why it is actually relatively difficult to get infected with viruses like HIV.