ArticleMolecular ecology2018
Large-effect loci affect survival in Tasmanian devils (Sarcophilus harrisii) infected with a transmissible cancer.
Article in Molecular ecology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- Boost or Bust? The Impact of Supplementation on Functional Genetic Diversity and Selective Processes in Tasmanian Devils.Molecular ecology · 2025Article
- The devil in more detail: Eco-evolutionary genomics of Tasmanian devil persistence despite range-wide spread of a fatal, transmissible cancer.PLoS pathogens · 2025Article
- Life-history trade-offs and reproductive strategies in Tasmanian devils following disease-induced population decline.Proceedings. Biological sciences · 2025Article
- Adaptive potential in the face of a transmissible cancer in Tasmanian devils.Molecular ecology · 2024Article
- Intergenomic signatures of coevolution between Tasmanian devils and an infectious cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Complex associations between cancer progression and immune gene expression reveals early influence of transmissible cancer on Tasmanian devils.Frontiers in immunology · 2024Article
- Article
- Restoring faith in conservation action: Maintaining wild genetic diversity through the Tasmanian devil insurance program.iScience · 2022Article
- Whole genome resequencing reveals signatures of rapid selection in a virus-affected commercial fishery.Molecular ecology · 2022Article
- Expression of the Nonclassical MHC Class I, Saha-UD in the Transmissible Cancer Devil Facial Tumour Disease (DFTD).Pathogens (Basel, Switzerland) · 2022Article
- Spatial variation in gene expression of Tasmanian devil facial tumors despite minimal host transcriptomic response to infection.BMC genomics · 2021Article
- Contemporary and historical selection in Tasmanian devils (Proceedings. Biological sciences · 2021Article
- Quantifying 25 years of disease-caused declines in Tasmanian devil populations: host density drives spatial pathogen spread.Ecology letters · 2021Article
- Darwin, the devil, and the management of transmissible cancers.Conservation biology : the journal of the Society for Conservation Biology · 2021Article
- Genomic association with pathogen carriage in bighorn sheep (Ecology and evolution · 2021Article
- Sarcoptic mange severity is associated with reduced genomic variation and evidence of selection in Yellowstone National Park wolves (Evolutionary applications · 2021Article
- Population genomics for wildlife conservation and management.Molecular ecology · 2021Review
- Infectious disease and sickness behaviour: tumour progression affects interaction patterns and social network structure in wild Tasmanian devils.Proceedings. Biological sciences · 2020Article
- Comparative landscape genetics reveals differential effects of environment on host and pathogen genetic structure in Tasmanian devils (Sarcophilus harrisii) and their transmissible tumour.Molecular ecology · 2020Article
- Disease swamps molecular signatures of genetic-environmental associations to abiotic factors in Tasmanian devil (Sarcophilus harrisii) populations.Evolution; international journal of organic evolution · 2020Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 3 countries.
Funding
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 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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