Mascheretti S, Croucher P J P, Vettraino A, Prospero S, Garbelotto M
Department of Environmental Science, Policy and Management, 137 Mulford Hall, University of California, Berkeley, CA 94720-3114, USA.
Mol Ecol. 2008 Jun;17(11):2755-68. doi: 10.1111/j.1365-294X.2008.03773.x. Epub 2008 Apr 23.
The genetic structure of the clonally reproducing Sudden Oak Death (SOD) pathogen in California was investigated using seven variable microsatellites. A total of 35 multilocus genotypes were identified among 292 samples representative of populations from 14 forest sites and of the nursery trade. amova indicated significant genetic variability both within (44.34%) and among populations (55.66%). Spatial autocorrelation analyses indicated that Moran's index of similarity reached a minimum of 0.1 at 350 m, increased to 0.4 at 1500 m and then decreased to zero at 10 km. These results suggest a bimodal pattern of spread, with medium range dispersal (1500-10,000 m) putatively attributed to the presence of strong winds. Lack of genetic structure was identified for three groups of populations. One group notably included the nurseries' population and two forest populations, both linked to early reports of the pathogen. A neighbour-joining analysis based on pairwise Phi(ST) values indicated that the clade inclusive of the nurseries' populations is basal to all California populations. A network analysis identified three common genotypes as the likely founders of the California infestation and proposes a stepwise model for local evolution of novel genotypes. This was supported by the identification in the same locations of novel genotypes and of their 1- or 2-step parents. We hypothesize that the few undifferentiated population groups indicate historical human spread of the pathogen, while the general presence of genetically structured populations indicates that new infestations are currently generated by rare medium or long-range natural movement of the pathogen, followed by local generation of new genotypes.
利用七个可变微卫星对加利福尼亚州克隆繁殖的橡树猝死病菌(SOD)病原体的遗传结构进行了研究。在代表14个森林地点和苗圃贸易的292个样本中,共鉴定出35种多位点基因型。分子方差分析(AMOVA)表明,群体内部(44.34%)和群体之间(55.66%)均存在显著的遗传变异。空间自相关分析表明,莫兰相似性指数在350米处达到最小值0.1,在1500米处增至0.4,然后在10公里处降至零。这些结果表明存在一种双峰传播模式,中程扩散(1500 - 10000米)据推测归因于强风的存在。三组群体未发现遗传结构。其中一组特别包括苗圃群体和两个森林群体,这两个群体均与该病原体的早期报告有关。基于成对Phi(ST)值的邻接法分析表明,包含苗圃群体的进化枝是所有加利福尼亚群体的基部。网络分析确定了三种常见基因型可能是加利福尼亚侵染的起源,并提出了新基因型局部进化的逐步模型。在相同地点鉴定出的新基因型及其一步或两步亲本为此提供了支持。我们假设,少数未分化的群体表明该病原体是由人类历史传播的,而遗传结构群体的普遍存在表明,目前新的侵染是由病原体罕见的中程或远程自然移动产生的,随后在当地产生新的基因型。