Genomic Signatures of Endemic Pathogen Exposure in a Declining Amphibian
Alexander S Wendt1, Lee Berger1, Lee F Skerratt1
1Melbourne Veterinary School, Faculty of Science, The University of Melbourne, Werribee, Victoria, Australia.
Abstract:
Endemic wildlife diseases can impose strong selection on threatened populations, yet whether persistence is associated with adaptive genomic responses remains poorly understood. We tested whether long-term exposure to Batrachochytrium dendrobatidis (Bd) following population declines has left detectable selection signatures in the genome of the alpine tree frog, Litoria verreauxii alpina. Because prior work suggests limited immunity to Bd within the species, we did not expect persistence to be explained primarily by repeated shifts at canonical immune genes. Instead, we expected pathogen-associated differentiation, if present, to be diffuse and weakly shared across contrasts, potentially involving regulatory, signalling or reproduction pathways consistent with tolerance, compensatory recruitment or demographic turnover. Using genome-wide SNP data, we compared Bd-naïve and Bd-endemic populations and two 11-year temporal resampling contrasts. Candidate SNPs were annotated to identify genomic context, nearby genes, putative functions and overlap with previously reported Bd-associated transcriptomic responses. Using an empirical 99th-percentile XtX threshold, scans identified high-differentiation candidate SNPs in all contrasts. Most occurred in noncoding and putatively regulatory regions, with relatively few canonical immune genes. Candidate-associated genes were more often linked to signalling, transcriptional regulation and cell-cycle processes. A descriptive comparison with previous work in the species identified 64 candidate-associated genes matching Bd-associated transcriptomic annotations, supporting several immune-adjacent, regulatory, cellular and reproduction candidates. Persistence under endemic Bd might reflect pathogen-associated selection, compensatory recruitment and demographic change following recurrent adult mortality rather than uniform adaptive rescue through immune resistance.


