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

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    MCCALLUM185299.pdf (819.2Kb)
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    Accepted Manuscript (AM)
    Author(s)
    Margres, Mark J
    Jones, Menna E
    Epstein, Brendan
    Kerlin, Douglas H
    Comte, Sebastien
    Fox, Samantha
    Fraik, Alexandra K
    Hendricks, Sarah A
    Huxtable, Stewart
    Lachish, Shelly
    Lazenby, Billie
    O'Rourke, Sean M
    Stahlke, Amanda R
    Wiench, Cody G
    Hamede, Rodrigo
    Schonfeld, Barbara
    McCallum, Hamish
    Miller, Michael R
    Hohenlohe, Paul A
    Storfer, Andrew
    Griffith University Author(s)
    McCallum, Hamish
    Year published
    2018
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    Abstract
    Identifying the genetic architecture of complex phenotypes is a central goal of modern biology, particularly for disease‐related traits. Genome‐wide 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 ...
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    Identifying the genetic architecture of complex phenotypes is a central goal of modern biology, particularly for disease‐related traits. Genome‐wide 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.
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    Journal Title
    MOLECULAR ECOLOGY
    Volume
    27
    Issue
    21
    DOI
    https://doi.org/10.1111/mec.14853
    Copyright Statement
    © 2018 John Wiley & Sons Ltd. This is the peer reviewed version of the following article: Large‐effect loci affect survival in Tasmanian devils (Sarcophilus harrisii) infected with a transmissible cancer, Molecular Ecology, Volume 27, Issue 21, which has been published in final form at https://doi.org/10.1111/mec.14853. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving (http://olabout.wiley.com/WileyCDA/Section/id-828039.html)
    Subject
    Biological sciences
    Publication URI
    http://hdl.handle.net/10072/383713
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    • Journal articles

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