Lachish S, Miller K J, Storfer A, Goldizen A W, Jones M E
School of Biological Sciences, University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Heredity (Edinb). 2011 Jan;106(1):172-82. doi: 10.1038/hdy.2010.17. Epub 2010 Mar 10.
Infectious disease has been shown to be a major cause of population declines in wild animals. However, there remains little empirical evidence on the genetic consequences of disease-mediated population declines, or how such perturbations might affect demographic processes such as dispersal. Devil facial tumour disease (DFTD) has resulted in the rapid decline of the Tasmanian devil, Sarcophilus harrisii, and threatens to cause extinction. Using 10 microsatellite DNA markers, we compared genetic diversity and structure before and after DFTD outbreaks in three Tasmanian devil populations to assess the genetic consequences of disease-induced population decline. We also used both genetic and demographic data to investigate dispersal patterns in Tasmanian devils along the east coast of Tasmania. We observed a significant increase in inbreeding (F(IS) pre/post-disease -0.030/0.012, P<0.05; relatedness pre/post-disease 0.011/0.038, P=0.06) in devil populations after just 2-3 generations of disease arrival, but no detectable change in genetic diversity. Furthermore, although there was no subdivision apparent among pre-disease populations (θ=0.005, 95% confidence interval (CI) -0.003 to 0.017), we found significant genetic differentiation among populations post-disease (θ=0.020, 0.010-0.027), apparently driven by a combination of selection and altered dispersal patterns of females in disease-affected populations. We also show that dispersal is male-biased in devils and that dispersal distances follow a typical leptokurtic distribution. Our results show that disease can result in genetic and demographic changes in host populations over few generations and short time scales. Ongoing management of Tasmanian devils must now attempt to maintain genetic variability in this species through actions designed to reverse the detrimental effects of inbreeding and subdivision in disease-affected populations.
传染病已被证明是野生动物种群数量下降的主要原因。然而，关于疾病介导的种群数量下降的遗传后果，或者这种扰动如何影响诸如扩散等种群动态过程，仍然缺乏实证证据。袋獾面部肿瘤病（DFTD）已导致袋獾（Sarcophilus harrisii）数量迅速减少，并有可能导致其灭绝。我们使用10个微卫星DNA标记，比较了三个袋獾种群在DFTD爆发前后的遗传多样性和结构，以评估疾病导致的种群数量下降的遗传后果。我们还利用遗传和种群动态数据，研究了塔斯马尼亚岛东海岸袋獾的扩散模式。我们观察到，在疾病出现仅2至3代后，袋獾种群的近亲繁殖显著增加（疾病前后的F(IS)分别为-0.030/0.012，P<0.05；疾病前后的亲缘关系分别为0.011/0.038，P=0.06），但遗传多样性没有可检测到的变化。此外，尽管在疾病发生前的种群之间没有明显的细分（θ=0.005，95%置信区间（CI）为-0.003至0.017），但我们发现疾病发生后的种群之间存在显著的遗传分化（θ=0.020，0.010 - 0.027），这显然是由选择和疾病影响种群中雌性扩散模式的改变共同驱动的。我们还表明，袋獾的扩散存在雄性偏向，且扩散距离遵循典型的尖峰分布。我们的结果表明，疾病可在几代和短时间尺度内导致宿主种群的遗传和种群动态变化。目前，对袋獾的持续管理必须试图通过采取行动来维持该物种的遗传变异性，以扭转疾病影响种群中近亲繁殖和细分的有害影响。
