Data from: Prelude to a panzootic: gene flow and immunogenetic variation in northern little brown myotis vulnerable to bat white-nose syndrome

The fungus that causes bat white-nose syndrome (WNS) recently leaped from
eastern North America to the Pacific Coast. The pathogen’s spread is
associated with the genetic population structure of a host (Myotis
lucifugus). To understand the fine-scale neutral and immunogenetic
variation among northern populations of M. lucifugus, we sampled 1142
individuals across the species’ northern range. We used genotypes at 11
microsatellite loci to reveal the genetic structure of, and directional
gene flow among, populations to predict the likely future spread of the
pathogen in the northwest and to estimate effective population size (Ne).
We also pyrosequenced the DRB1-like exon 2 of the class II major
histocompatibility complex (MHC) in 160 individuals to explore
immunogenetic selection by WNS. We identified three major neutral genetic
clusters: Eastern, Montane Cordillera (and adjacent sampling areas), and
Haida Gwaii, with admixture at intermediate areas and significant
substructure west of the prairies. Estimates of Ne were unexpectedly low
(289–16 000). Haida Gwaii may provide temporary refuge from WNS, but the
western mountain ranges are not barriers to its dispersal in M. lucifugus
and are unlikely to slow its spread. Our major histocompatibility complex
(MHC) data suggest potential selection by WNS on the MHC, but gene
duplication limited the immunogenetic analyses.