Author
Listed:
- Brendan Epstein
(School of Biological Sciences, Washington State University)
- Menna Jones
(School of Zoology, University of Tasmania)
- Rodrigo Hamede
(School of Zoology, University of Tasmania)
- Sarah Hendricks
(Institute for Bioinformatics and Evolutionary Studies, University of Idaho)
- Hamish McCallum
(School of Environment, Griffith University, Nathan Campus)
- Elizabeth P. Murchison
(University of Cambridge)
- Barbara Schönfeld
(School of Zoology, University of Tasmania)
- Cody Wiench
(Institute for Bioinformatics and Evolutionary Studies, University of Idaho)
- Paul Hohenlohe
(Institute for Bioinformatics and Evolutionary Studies, University of Idaho)
- Andrew Storfer
(School of Biological Sciences, Washington State University)
Abstract
Although cancer rarely acts as an infectious disease, a recently emerged transmissible cancer in Tasmanian devils (Sarcophilus harrisii) is virtually 100% fatal. Devil facial tumour disease (DFTD) has swept across nearly the entire species’ range, resulting in localized declines exceeding 90% and an overall species decline of more than 80% in less than 20 years. Despite epidemiological models that predict extinction, populations in long-diseased sites persist. Here we report rare genomic evidence of a rapid, parallel evolutionary response to strong selection imposed by a wildlife disease. We identify two genomic regions that contain genes related to immune function or cancer risk in humans that exhibit concordant signatures of selection across three populations. DFTD spreads between hosts by suppressing and evading the immune system, and our results suggest that hosts are evolving immune-modulated resistance that could aid in species persistence in the face of this devastating disease.
Suggested Citation
Brendan Epstein & Menna Jones & Rodrigo Hamede & Sarah Hendricks & Hamish McCallum & Elizabeth P. Murchison & Barbara Schönfeld & Cody Wiench & Paul Hohenlohe & Andrew Storfer, 2016.
"Rapid evolutionary response to a transmissible cancer in Tasmanian devils,"
Nature Communications, Nature, vol. 7(1), pages 1-7, November.
Handle:
RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12684
DOI: 10.1038/ncomms12684
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