Biology subjects

Murphy, H. A.

Publications and source records attributed to Murphy, H. A..

3 recordsLinked to original sources

bioRxiv2022

The effect of recognition on competition among clones in spatially structured microbial communities

In spatially structured microbial communities, clonal growth of stationary cells passively generates clusters of related cells. This can lead to stable cooperation without the need for recognition mechanisms. However, recent research suggests that some biofilm-forming microbes may have mechanisms of kin recognition. To explore this unexpected observation, we studied the effects of different types of cooperation in a microbial colony using spatially explicit, agent-based simulations of two interacting strains. We found scenarios that favor a form of kin recognition in spatially structured microbial communities. In the presence of a "cheater" strain, strains with greenbeard cooperation was able to increase in frequency more than obligate cooperators. This effect was most noticeable in high density colonies and when the cooperators were not as abundant as the cheaters. We also studied whether a polychromatic greenbeard, in which cells only cooperate with their own type, could provide a numerical benefit beyond a simple, binary greenbeard. We found the greatest benefit to a polychromatic greenbeard when cooperation is highly effective. These results suggest that in some ecological scenarios, recognition mechanisms may be beneficial even in spatially structured communities.

evolutionary biology↗

bioRxiv2022

Selection on plastic adherence leads to hyper-multicellular strains and incidental virulence in the budding yeast

Many disease-causing microbes are not obligate pathogens; rather, they are environmental microbes taking advantage of an ecological opportunity. The existence of microbes that are not normally pathogenic, yet are well-suited to host exploitation, is an evolutionary paradox. One hypothesis posits that selection in the environment may favor traits that incidentally lead to pathogenicity and virulence, or serve as pre-adaptations for survival in a host. An example of such a trait is surface adherence. To experimentally test the idea of "accidental virulence", replicate populations of the yeast, Saccharomyces cerevisiae, which can be an opportunistic pathogen, were evolved to attach to a plastic bead for hundreds of generations. Along with plastic adherence, two multicellular phenotypes-- biofilm formation and flor formation-- increased; another phenotype, pseudohyphal growth, responded to the nutrient limitation. Thus, experimental selection led to the evolution of highly-adherent, hyper-multicellular strains. Wax moth larvae injected with evolved hyper-multicellular strains were significantly more likely to die than those injected with evolved non-multicellular strains. Hence, selection on plastic adherence incidentally led to the evolution of enhanced multicellularity and increased virulence. Our results support the idea that selection in the environment for a trait unrelated to virulence can inadvertently generate opportunistic, "accidental" pathogens.

evolutionary biology↗

bioRxiv2016

The effect of known mutator alleles in a cluster of clinical Saccharomyces cerevisiae strains

Natural selection has the potential to act on all phenotypes, including genomic mutation rate. Classic evolutionary theory predicts that in asexual populations, mutator alleles, which cause high mutation rates, can fix due to linkage with beneficial mutations. This phenomenon has been demonstrated experimentally and may explain the frequency of mutators found in bacterial pathogens. In contrast, in sexual populations, recombination decouples mutator alleles from beneficial mutations, preventing mutator fixation. In the facultatively sexual yeast Saccharomyces cerevisiae, segregating alleles of MLH1 and PMS1 have been shown to be incompatible, causing a high mutation rate when combined. These alleles had never been found together naturally, but were recently discovered in a cluster of clinical isolates. Here we report that the incompatible mutator allele combination only marginally elevates mutation rate in these clinical strains. Genomic and phylogenetic analyses provide no evidence of a historically elevated mutation rate. We conclude that the effect of the mutator alleles is dampened by background genetic modifiers. Thus, the relationship between mutation rate and microbial pathogenicity may be more complex than once thought. Our findings provide rare observational evidence that supports evolutionary theory suggesting that sexual organisms are unlikely to harbor alleles that increase their genomic mutation rate.

evolutionary biology↗