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Whole genome resequencing reveals signatures of rapid selection in a virus affected commercial fishery
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  • Owen Holland,
  • Madeline Toomey,
  • Collin Ahrens,
  • Ary Hoffmann,
  • Larry Kroft,
  • Craig Sherman,
  • Adam Miller
Owen Holland
Deakin University
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Madeline Toomey
Deakin University
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Collin Ahrens
Western Sydney University
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Ary Hoffmann
The University of Melbourne
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Larry Kroft
Deakin University
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Craig Sherman
Deakin University
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Adam Miller
Deakin University - Geelong Campus at Waurn Ponds
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Abstract

Infectious diseases are recognised as one of the greatest global threats to biodiversity and ecosystem functioning. Consequently, there is a growing urgency to understand the speed at which adaptive phenotypes can evolve and spread in natural populations to inform future management. Here we provide evidence of rapid genomic changes in wild Australian blacklip abalone (Haliotis rubra) following a major population crash associated with an infectious disease. A genome wide association study on H. rubra was conducted using pooled whole genome re-sequencing data from commercial fishing stocks varying in historical exposure to haliotid herpesvirus-1 (HaHV-1). Approximately 25,000 SNP loci associated with virus exposure were identified, many of which mapped to genes known to contribute to HaHV-1 immunity in the New Zealand pāua (H. iris) and herpesvirus response pathways in haliotids and other animal systems. These findings indicate genetic changes across a single generation in H. rubra fishing stocks decimated by HaHV-1, with stock recovery determined by rapid evolutionary changes leading to virus resistance. This is a novel example of rapid adaptation in natural populations of a non-model marine organism, highlighting the pace at which selection can potentially act to counter disease in wildlife communities.