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Disease swamps molecular signatures of genetic‐environmental associations to abiotic factors in Tasmanian devil ( Sarcophilus harrisii ) populations
Evolution ( IF 3.1 ) Pub Date : 2020-06-03 , DOI: 10.1111/evo.14023
Alexandra K Fraik 1 , Mark J Margres 1 , Brendan Epstein 1, 2 , Soraia Barbosa 3 , Menna Jones 4 , Sarah Hendricks 3 , Barbara Schönfeld 4 , Amanda R Stahlke 3 , Anne Veillet 3 , Rodrigo Hamede 4 , Hamish McCallum 5 , Elisa Lopez-Contreras 1 , Samantha J Kallinen 1 , Paul A Hohenlohe 3 , Joanna L Kelley 1 , Andrew Storfer 1
Affiliation  

Landscape genomics studies focus on identifying candidate genes under selection via spatial variation in abiotic environmental variables, but rarely by biotic factors (i.e., disease). The Tasmanian devil (Sarcophilus harrisii) is found only on the environmentally heterogeneous island of Tasmania and is threatened with extinction by a transmissible cancer, devil facial tumor disease (DFTD). Devils persist in regions of long‐term infection despite epidemiological model predictions of species’ extinction, suggesting possible adaptation to DFTD. Here, we test the extent to which spatial variation and genetic diversity are associated with the abiotic environment (i.e., climatic variables, elevation, vegetation cover) and/or DFTD. We employ genetic‐environment association analyses using 6886 SNPs from 3287 individuals sampled pre‐ and post‐disease arrival across the devil's geographic range. Pre‐disease, we find significant correlations of allele frequencies with environmental variables, including 365 unique loci linked to 71 genes, suggesting local adaptation to abiotic environment. The majority of candidate loci detected pre‐DFTD are not detected post‐DFTD arrival. Several post‐DFTD candidate loci are associated with disease prevalence and were in linkage disequilibrium with genes involved in tumor suppression and immune response. Loss of apparent signal of abiotic local adaptation post‐disease suggests swamping by strong selection resulting from the rapid onset of DFTD.

中文翻译:

疾病沼泽与塔斯马尼亚恶魔 (Sarcophilus harrisii) 种群中非生物因素的遗传环境关联的分子特征

景观基因组学研究的重点是通过非生物环境变量的空间变化来确定选择的候选基因,但很少通过生物因素(即疾病)。塔斯马尼亚恶魔 (Sarcophilus harrisii) 仅在环境异质的塔斯马尼亚岛上发现,并且受到传染性癌症、恶魔面部肿瘤病 (DFTD) 的威胁而灭绝。尽管流行病学模型预测物种灭绝,但恶魔仍然存在于长期感染的地区,这表明可能适应 DFTD。在这里,我们测试空间变异和遗传多样性与非生物环境(即气候变量、海拔、植被覆盖)和/或 DFTD 相关的程度。我们使用来自 3287 个个体的 6886 个 SNP 进行遗传-环境关联分析,这些个体在病前和病后到达魔鬼的地理范围内采样。发病前,我们发现等位基因频率与环境变量显着相关,包括与 71 个基因相关的 365 个独特位点,表明对非生物环境的局部适应。大多数在 DFTD 前检测到的候选位点在 DFTD 到达后未检测到。几个后 DFTD 候选位点与疾病流行相关,并且与参与肿瘤抑制和免疫反应的基因存在连锁不平衡。非生物局部适应病后明显信号的丧失表明,由于 DFTD 的快速发作,强选择造成了淹没。我们发现等位基因频率与环境变量显着相关,包括与 71 个基因相关的 365 个独特位点,表明对非生物环境的局部适应。大多数在 DFTD 前检测到的候选位点在 DFTD 到达后未检测到。几个后 DFTD 候选位点与疾病流行相关,并且与参与肿瘤抑制和免疫反应的基因存在连锁不平衡。非生物局部适应病后明显信号的丧失表明,由于 DFTD 的快速发作,强选择造成了淹没。我们发现等位基因频率与环境变量显着相关,包括与 71 个基因相关的 365 个独特位点,表明对非生物环境的局部适应。大多数在 DFTD 前检测到的候选位点在 DFTD 到达后未检测到。几个后 DFTD 候选位点与疾病流行相关,并且与参与肿瘤抑制和免疫反应的基因存在连锁不平衡。非生物局部适应病后明显信号的丧失表明,由于 DFTD 的快速发作,强选择造成了淹没。几个后 DFTD 候选位点与疾病流行相关,并且与参与肿瘤抑制和免疫反应的基因存在连锁不平衡。非生物局部适应病后明显信号的丧失表明,由于 DFTD 的快速发作,强选择造成了淹没。几个后 DFTD 候选位点与疾病流行相关,并且与参与肿瘤抑制和免疫反应的基因存在连锁不平衡。非生物局部适应病后明显信号的丧失表明,由于 DFTD 的快速发作,强选择造成了淹没。
更新日期:2020-06-03
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