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Large-effect loci affect survival in Tasmanian devils (Sarcophilus harrisii) infected with a transmissible cancer

Margres, MJ, Jones, ME ORCID: 0000-0001-7558-9022, Epstein, B, Kerlin, DH, Comte, S ORCID: 0000-0001-7984-8159, Fox, S, Fraik, AK, Hendricks, SA, Huxtable, S, Lachish, S, Lazenby, B, O'Rourke, SM, Stahlke, AR, Wiench, CG, Hamede, R ORCID: 0000-0003-1526-225X, Schonfeld, B, McCallum, H, Miller, MR, Hohenlohe, PA and Storfer, A 2018 , 'Large-effect loci affect survival in Tasmanian devils (Sarcophilus harrisii) infected with a transmissible cancer' , Molecular Ecology, vol. 27, no. 21 , pp. 4189-4199 , doi: 10.1111/mec.14853.

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Abstract

association methods are a classical approach for identifying the genomic basis of variation in disease phenotypes, but such analyses are particularly challenging in natural populations due to sample size difficulties. Extensive mark-recapture data, strong linkage disequilibrium and a lethal transmissible cancer make the Tasmanian devil (Sarcophilus harrisii) an ideal model for such an association study. We used a RAD-capture approach to genotype 624 devils at ∼16,000 loci and then used association analyses to assess the heritability of three cancer‐related phenotypes: infection case-control (where cases were infected devils and controls were devils that were never infected), age of first infection and survival following infection. The SNP array explained much of the phenotypic variance for female survival (> 80%) and female case–control (> 61%). We found that a few large‐effect SNPs explained much of the variance for female survival (∼5 SNPs explained > 61% of the total variance), whereas more SNPs (∼56) of smaller effect explained less of the variance for female case-control (∼23% of the total variance). By contrast, these same SNPs did not account for a significant proportion of phenotypic variance in males, suggesting that the genetic bases of these traits and/or selection differ across sexes. Loci involved with cell adhesion and cell‐cycle regulation underlay trait variation, suggesting that the devil immune system is rapidly evolving to recognize and potentially suppress cancer growth through these pathways. Overall, our study provided necessary data for genomics‐based conservation and management in Tasmanian devils.

Item Type: Article
Authors/Creators:Margres, MJ and Jones, ME and Epstein, B and Kerlin, DH and Comte, S and Fox, S and Fraik, AK and Hendricks, SA and Huxtable, S and Lachish, S and Lazenby, B and O'Rourke, SM and Stahlke, AR and Wiench, CG and Hamede, R and Schonfeld, B and McCallum, H and Miller, MR and Hohenlohe, PA and Storfer, A
Keywords: Tasmanian devil, devil facial tumour disease, wildlife disease
Journal or Publication Title: Molecular Ecology
Publisher: Blackwell Publishing Ltd
ISSN: 0962-1083
DOI / ID Number: 10.1111/mec.14853
Copyright Information:

© 2018 John Wiley & Sons Ltd.

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