David Clark & Karen Peralta Martinez
Causes of variation in the distribution and virulence of parasites among hosts (Clark)
Parasites are ubiquitous and occur in a majority of natural systems, but they do not interact with all hosts equally. Host-parasite interactions can vary at species, population or the individual level. This variation leads to key differences in how parasites are distributed among hosts, the costs they impose on their hosts, or how well they transmit among individuals within populations. Identifying key factors that contribute to this variation can better help us understand how and why parasites are successful within natural populations. Here, we propose that differences in host behavior can lead to variation in how parasites are distributed among their hosts and the damage they inflict on their hosts (‘virulence’). We use a Trinidadian guppy (Poecilia reticulata) and Gyrodactylus spp. parasite system to test this hypothesis. We found that, across 57 wild populations, parasites are more aggregated among female than among male hosts, potentially due to sex differences in host behavior. As well as the distribution of parasites, behavior may drive population-level differences in parasite virulence. Host populations subject to higher predation pressure are more social as a defense against predators, providing more transmission opportunities for the parasite. In the lab, consistent with theoretical predictions, parasites from more social host populations reach higher infection loads, and their hosts are less likely to recover. Overall, these results highlight how differences in host traits can cause variation in how they interact with their parasites.
Understanding microbial contribution to host phenotypic plasticity (Peralta Martinez)
The vertebrate gastrointestinal tract is a flexible system that is highly responsive to internal (host) and external (environment) dynamics. Our understanding of this plasticity, both biomedically relevant and in the context of ecology and evolution, has largely been studied without considering the gut microbiome – the diverse microbial communities that perform vital physiological and metabolic functions. Diet induces changes in the form and function of the gastrointestinal tract, and the microbial community within. However, the microbial contribution to the rapid and reversible changes in the physiology of the gastrointestinal tract remains unexplored. The products of bacterial fermentation, also known as short-chain fatty acids, act as energy sources, histone deacetylase (HDAC) inhibitors, and G-protein coupled receptor molecules in various cells. I hypothesize that short-chain fatty acids modulate gene expression via epigenetic controls to alter rapid adaptations in the gastrointestinal tract. For my dissertation research, I will test whether the microbiome (via the production of short-chain fatty acids) alters host plasticity and gene expression. I plan to integrate aspects of protein activity and expression, host transcriptomics, and microbial metagenomics, and epigenetics to understand the relationship between diet, microbiome, and host in the gastrointestinal tract system with a focus on animal’s ecology and evolution.
Wednesday, September 2, 2020
A219B Langley Hall or via ZOOM