TY - JOUR
T1 - Rapid evolutionary response to a transmissible cancer in Tasmanian devils
AU - Epstein, Brendan
AU - Jones, Menna
AU - Hamede, Rodrigo
AU - Hendricks, Sarah
AU - McCallum, Hamish
AU - Murchison, Elizabeth P.
AU - Sch�nfeld, Barbara
AU - Wiench, Cody
AU - Hohenlohe, Paul
AU - Storfer, Andrew
N1 - Publisher Copyright:
© The Author(s) 2016.
PY - 2016/8/30
Y1 - 2016/8/30
N2 - 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.
AB - 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.
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U2 - 10.1038/ncomms12684
DO - 10.1038/ncomms12684
M3 - Article
C2 - 27575253
AN - SCOPUS:84984998175
SN - 2041-1723
VL - 7
JO - Nature communications
JF - Nature communications
M1 - 12684
ER -