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Ford, S. A.

Publications and source records attributed to Ford, S. A..

3 recordsLinked to original sources

Salt stress alters the spectrum of de novo mutation available to selection during experimental adaptation of Chlamydomonas reinhardtii

The genetic basis of adaptation is driven not only by selection, but also by the spectrum of available mutations. Given that the rate of mutation is not uniformly distributed across the genome and varies depending on the environment, understanding the signatures of selection across the genome is aided by first establishing what the expectations of genetic change are from mutation. To determine the interaction between salt stress, selection, and mutation across the genome, we compared the rates and patterns of mutation observed in a selection experiment for salt tolerance in Chlamydomonas reinhardtii to those observed in mutation accumulation experiments with and without salt exposure. We found that salt stress led to an increased rate of indel mutations, but that many of these mutations were removed under selection. Finally, lines adapted to salt also showed excess clustering of mutations in the genome and the co-expression network, suggesting a role for positive selection in retaining mutations in particular compartments of the genome during the evolution of salt tolerance. Our study shows that characterizing mutation rates and spectra expected under stress helps disentangle the effects of environment and selection during adaptation.

evolutionary biology↗

Protective microbe enhances colonisation of a novel host species by modifying immune gene expression

Microbes that protect against infection inhabit hosts across the tree of life. It is unclear whether many protective microbes use or reduce the need for a host immune response, or how the immune system reacts when these microbes newly encounter a host species naturally and as part of a biocontrol strategy. We sequenced the transcriptome of a host (Caenorhabditis elegans) following its interaction with a non-native bacterium (Enterococcus faecalis) that has protective traits against the pathogen, Staphylococcus aureus. We show that microbe-mediated protection caused the differential expression of 1,557 genes, including the upregulation of many immune gene families conserved across the animal kingdom (e.g. lysozymes and c-type lectins). We found that this modulation of the hosts immune response was beneficial for both the protective microbe and the host. Given E. faecalis increased ability to resist lysozyme activity compared to S. aureus, our results indicate that the protective microbe could more easily invade and protect infected hosts by upregulating lysozyme genes. These results suggest that a protective microbe can exploit the host immune system even when introduced into a novel species. Microbes that protect via the host immune response in this way should favour continued investment into host immunity and avoid the evolution of host dependence. Author summaryOrganisms can be protected from infectious disease by the microbes they house. It is unclear, however, whether protective microbes affect the host immune response to infection, particularly in the early stages of symbiosis. In this study, we investigated the role of the host immune system in a novel protective interaction. We examined gene expression in a nematode after colonisation by a non-native microbe capable of suppressing the pathogen Staphylococcus aureus. The protective microbe altered the host immune response to infection in a way that it could exploit. By causing the host to increase the production of antimicrobials to which it itself is relatively resistant, the protective microbe was better able to colonise and defend infected hosts. These results indicate that protective microbes introduced into new host species can take advantage of the host immune system. Such a mechanism at the beginning of a protective symbiosis, formed either naturally or as part of a biocontrol strategy, could ensure continued investment in host-based defences over evolutionary time.

microbiology↗

Artificial selection finds new hypotheses for the mechanism of Wolbachia-mediated dengue blocking in mosquitoes

Wolbachia is an intracellular bacterium that blocks virus replication in insects and has been introduced into the mosquito, Aedes aegypti for the biocontrol of arboviruses including dengue, Zika and chikungunya. Despite ongoing research, the mechanism of Wolbachia-mediated virus blocking remains unclear. We recently used experimental evolution to reveal that Wolbachia-mediated dengue blocking could be selected upon in the A. aegypti host and showed evidence that strong levels of blocking could be maintained by natural selection. In this study, we investigate the genetic variation associated with blocking and use these analyses to generate testable hypotheses surrounding the mechanism of Wolbachia-mediated dengue blocking. From our results, we hypothesise that Wolbachia may block virus replication by increasing the regeneration rate of mosquito cells via the Notch signalling pathway. We also propose that Wolbachia modulates the hosts transcriptional pausing pathway either to prime the hosts anti-viral response or to directly inhibit viral replication.

evolutionary biology↗