Abstract
Yersinia pestis was introduced to North America around 1900 and leads to nearly 100% mortality in prairie dog (Cynomys spp.) colonies during epizootic events, which suggests this pathogen may exert a strong selective force. We characterized genetic diversity at an MHC class II locus (DRB1) in Gunnison's prairie dog (C. gunnisoni) and quantified population genetic structure at the DRB1 versus 12 microsatellite loci in three large Arizona colonies. Two colonies, Seligman (SE) and Espee Ranch (ES), have experienced multiple plague‐related die‐offs in recent years, whereas plague has never been documented at Aubrey Valley (AV). We found fairly low allelic diversity at the DRB1 locus, with one allele (DRB1*01) at high frequency (0.67–0.87) in all colonies. Two other DRB1 alleles appear to be trans‐species polymorphisms shared with the black‐tailed prairie dog (C. ludovicianus), indicating that these alleles have been maintained across evolutionary time frames. Estimates of genetic differentiation were generally lower at the MHC locus (F ST = 0.033) than at microsatellite markers (F ST = 0.098). The reduced differentiation at DRB1 may indicate that selection has been important for shaping variation at MHC loci, regardless of the presence or absence of plague in recent decades. However, genetic drift has probably also influenced the DRB1 locus because its level of differentiation was not different from that of microsatellites in an F ST outlier analysis. We then compared specific MHC alleles to plague survivorship in 60 C. gunnisoni that had been experimentally infected with Y. pestis. We found that survival was greater in individuals that carried at least one copy of the most common allele (DRB1*01) compared to those that did not (60% vs. 20%). Although the sample sizes of these two groups were unbalanced, this result suggests the possibility that this MHC class II locus, or a nearby linked gene, could play a role in plague survival.
Highlights
Infectious diseases can play an important role in shaping genetic variation and fitness in free-living populations (Anderson and May 1979; Keller and Waller 2002; Keesing et al 2010)
Ecology and Evolution published by John Wiley & Sons Ltd
We found weak evidence for positive selection acting on the DRB1 locus in the black-tailed prairie dog, but not in Gunnison’s prairie dog, which may be a result of recent population reductions or the short time frame during which plague has been acting as a selective force
Summary
Infectious diseases can play an important role in shaping genetic variation and fitness in free-living populations (Anderson and May 1979; Keller and Waller 2002; Keesing et al 2010). Diseases may decrease allelic variation at immune system loci via selective sweeps (de Groot et al 2002; Carnero-Montoro et al 2012) and reduce variation at neutral loci as a result of genetic bottlenecks (Maruyama and Fuerst 1985; Luikart and Cornuet 1998). A cyclic pattern of rare allele advantage under pressure by coevolving pathogens (an evolutionary arms race) should result in the maintenance of a greater number of alleles over time due to balancing selection (Bodmer 1972; Potts and Wakeland 1990; Slade and McCallum 1992).
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