Data and code from: A multifaceted approach reveals complex genomic mediation of white-nose syndrome resistance in the little brown bat (Myotis lucifugus)

Novel pathogens have become a major challenge faced by wildlife in the Anthropocene. White-nose syndrome (WNS), a fungal pathogen, has decimated bat populations across North America over the last two decades. Demographic and physiological evidence of resistance in one heavily affected species, Myotis lucifugus, has prompted multiple attempts to delineate the genomic underpinnings, but they show little congruence in their findings. This may be due, in part, to the limitations of the genomic resources utilized and/or analytical approaches employed. Here, we performed high-coverage whole-genome resequencing of M. lucifugus sampled prior to (n = 29) and 10 years after the arrival of WNS (n = 30), aligned to a new reference genome to identify signatures of selection associated with pathogen resistance. Using 41.9 million SNPs, we implemented a combination of hard and soft sweep detection analyses, leading to discovery of 405 genes with robust evidence of selection. Of these, 241 (59.5 %) were associated with enriched gene ontology (GO) terms, many of which were tied to neuron development, organization, and function. Further, approximately half (120) of genes associated with enriched GO terms interact with genes identified by previous studies. Our findings suggest WNS resistance is mediated through highly complex, polygenic mechanisms. Further, we demonstrate there are far more connections among WNS selection study results than previously recognized. We believe that the methods employed by our study illustrate a need for a paradigm shift in non-model selection studies and further highlight the value of genomics as a tool for conservation management.