abstract
Bacteria and archaea reproduce clonally (vertical descent), but exchange genes by recombination (horizontal transfer). Recombination allows adaptive mutations or genes to spread rapidly within (or even between) species, and reduces the burden of deleterious mutations. Clonality – defined here as the balance between vertical and horizontal inheritance – is therefore a key microbial trait, determining how quickly a population can adapt and the size of its gene pool. Here, I discuss whether clonality varies over time and if it can be considered a stable trait of a given population. I show that, in some cases, clonality is clearly not static. For example, non-clonal (highly recombining) populations can give rise to clonal expansions, often of pathogens. However, an analysis of time-course metagenomic data from a lake suggests that a bacterial population’s past clonality (as measured by its genetic diversity) is a good predictor of its future clonality. Clonality therefore appears to be relatively – but not completely – stable over evolutionary time.
Footnotes
* jesse.shapiro{at}umontreal.ca
* A comprehensive discussion of the roles of selection and recombination in structuring microbial diversity.
* Deep sequencing of 90 cyanobacterial marker genes reveals extensive recombination, with each genome composed of a random mix of alleles from the gene pool.
* In-depth population genomic evidence of a panmictic ocean gene pool containing non-clonal ecological populations.
* Mathematical modeling shows how individual genes can sweep through populations with low recombination rates in the presence of negative frequency-dependent selection.
* A clear demonstration that genes in the integron are recombined between species just as often as within species, and that 24% of ‘core’ genes have crossed species boundaries.
** A pioneering application of time-course metagenomics to infer genome-wide and gene-specific selective sweeps in natural lake bacterial populations.
* The first simulation of bacterial evolution including mutation, allelic exchange (homologous recombination) and gene gain/loss (non-homologous recombination).
