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Hoff, S.

Publications and source records attributed to Hoff, S..

2 recordsLinked to original sources

Environmental conditions drive selection and recovery following disease-induced declines

Emerging infectious diseases threaten public health and biodiversity across the globe1,2. Disease outcomes are frequently dependent on local environmental conditions3-5, but how these factors shape host adaptation and long-term recovery are often unknown6. Here we combine two decades of population, disease, and environmental data with a common garden experiment to investigate the drivers of variable declines and recovery for remnant bat populations following the emergence of the fungal disease, white-nose syndrome. We find that initial declines were greater and faster in warmer sites (88.3% vs. 74.2% in cold sites), but these populations recovered more quickly and hosts developed higher resistance (1.5x reduction of fungal loads) than populations from colder sites that were buffered from initial impacts. Our experimental data suggest that warm sites served as hotspots of host adaptation where selective pressures were stronger because thermal conditions approached optimal growth for the pathogen, which eventually favored the development of high pathogen resistance. Populations in colder sites experienced weaker selective pressure and thus remain more susceptible, although bats from larger colonies were more likely to survive, suggesting that adaptive traits exist in these populations, but at much lower frequency. These findings show that the environmental conditions that initially buffer populations from collapse can simultaneously constrain their evolutionary response to emerging threats, and ultimately determine differential recovery following disease-induced declines.

ecology↗

Genome-wide changes in genetic diversity in a Myotis lucifugus population affected by white-nose syndrome

Novel pathogens can cause massive declines in populations, and even extirpation of hosts. But disease can also act as a selective pressure on survivors, driving the evolution of resistance or tolerance. Bat white-nose syndrome (WNS) is a rapidly spreading wildlife disease in North America. The fungus causing the disease invades skin tissues of hibernating bats, resulting in disruption of hibernation behavior, premature energy depletion, and subsequent death. We used whole-genome sequencing to investigate changes in allele frequencies within a population of Myotis lucifugus in eastern North America to search for genetic resistance to WNS. Our results show low FST values within the population across time, i.e. prior to WNS (Pre-WNS) compared to the population that has survived WNS (Post-WNS). However, when dividing the population with a geographical cut-off between the states of Pennsylvania and New York, a sharp increase in values on scaffold GL429776 is evident in the Post-WNS samples. Genes present in the diverged area are associated with thermoregulation and promotion of brown fat production. Thus, although WNS may not have subjected the entire M. lucifugus population to selective pressure, it may have selected for specific alleles in Pennsylvania through decreased gene flow within the population. However, the persistence of remnant sub-populations in the aftermath of WNS is likely due to multiple factors in bat life history.

evolutionary biology↗