Abstract

The degree to which species can rapidly adapt is key to survival in the face of climatic and other anthropogenic changes. For little brown bats (Myotis lucifugus), whose populations have experienced declines of over 90% because of the introduced fungal pathogen that causes white-nose syndrome (WNS), survival of the species may ultimately depend upon its capacity for adaptive change. Here, we present evidence of selectively driven change (adaptation), despite dramatic nonadaptive genomic shifts (genetic drift) associated with population declines. We compared the genetic makeups of wild survivors versus non-survivors of WNS, and found significant shifts in allele frequencies of genes associated with regulating arousal from hibernation (GABARB1), breakdown of fats (cGMP-PK1), and vocalizations (FOXP2). Changes at these genes are suggestive of evolutionary adaptation, given that WNS causes bats to arouse with unusual frequency from hibernation, contributing to premature depletion of fat reserves. However, whether these putatively adaptive shifts in allele frequencies translate into sufficient increases in survival for the species to rebound in the face of WNS is unknown.

Highlights

  • The degree to which species can rapidly adapt is key to survival in the face of climatic and other anthropogenic changes

  • We detected the effects of stochastic, non-adaptive genomic changes in otherwise neutral portions of the genome reflective of the large numbers that have died from white-nose syndrome (WNS) in this species

  • What the outcome of the evolutionary change we report here might be and what it bodes for the future recovery of little brown bats is not clear—it is too soon to claim that the species will be “saved” via an evolutionary rescue effect

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Summary

Introduction

The degree to which species can rapidly adapt is key to survival in the face of climatic and other anthropogenic changes. For little brown bats (Myotis lucifugus), whose populations have experienced declines of over 90% because of the introduced fungal pathogen that causes white-nose syndrome (WNS), survival of the species may depend upon its capacity for adaptive change. We compared the genetic makeups of wild survivors versus non-survivors of WNS, and found significant shifts in allele frequencies of genes associated with regulating arousal from hibernation (GABARB1), breakdown of fats (cGMP-PK1), and vocalizations (FOXP2) Changes at these genes are suggestive of evolutionary adaptation, given that WNS causes bats to arouse with unusual frequency from hibernation, contributing to premature depletion of fat reserves. Whether these putatively adaptive shifts in allele frequencies translate into sufficient increases in survival for the species to rebound in the face of WNS is unknown. Dramatic population losses may confound the effectiveness of selection or purge potential adaptive variants via genetic drift

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