基于全基因组重测序的中国猕猴桃溃疡病菌遗传多样性分析

 由Pseudomonas syringae pv. actinidiae (Psa)引起的猕猴桃细菌性溃疡病是为害猕猴桃的一种毁灭性病害,1996年被列为我国森林植物检疫对象。本研究对来源于我国7个受溃疡病为害最严重地区的21个Psa菌株进行重测序分析,通过主成分分析和系统发育学分析将21个菌株分为三大类群;固定系数分析结果显示所有群体的F_ST值均小于0.05;核苷酸多态性分析结果显示所有菌株的Θπ值仅为3.74×10^-6,且各群体间的差异不明显。这些结果表明Psa在我国的遗传多样性处于低水平状态。基因流(Nm)分析结果显示不同群体之间的Nm值均大于4,表明各群体病原菌之间存在较大的基因交流;Tajima′s D中性检验结果显示所有群体的Tajima′s D值均大于0,暗示各群体都经历平衡选择;Ka/Ks分析结果显示Psa的大部分基因都受到纯化选择,仅有极少数的基因受到正选择。本研究揭示了中国7个受溃疡病危害最严重地区Psa的遗传多样性,并且获得大量基因组数据,可为病害防治、病原菌耐药性以及抗病植株的选育提供理论依据。

Genetic diversity analysis of the kiwifruit canker pathogen in China based on whole genome resequencing

Bacterial canker of kiwifruit, caused by Pseudomonas syringae pv. actinidiae (Psa), is the most damaging disease of kiwifruit worldwide. It has been listed as a forest plant quarantine object in China in 1996. A total of 21 strains from the seven areas in China with most severe infection of bacterial canker were selected for resequencing and subjected to an in-depth analysis of genetic diversity among these strains. Principal component analysis (PCA) and phylogenetic analysis divided the 21 samples into three groups. Analysis of the degree of differentiation among the different regions using fixed coefficient (F_ST) showed that all F_ST values were less than 0.05. Nucleotide polymorphism analysis revealed that the Θπ value of 21 samples was only 3.74×10^-6, and the difference between the populations was not obvious. These findings indicate that the genetic diversity of Psa in China is at a low level. Gene flow analysis showed that the Nm values between different populations were greater than 4, revealing that there were substantial genetic exchanges between different populations. Tajima′s D values for all populations were greater than 0 which indicated that all populations were subject to balancing selection. Calculation of Ka/Ks indicated that most Psa genes are subject to purifying selection, whereas a few genes are under positive selection. This study reveals the genetic diversity of Psa in seven regions in China, and provides a large amount of Psa genomic data, which could offer a theoretical basis for further in-depth studies of the pathogenic mechanism of Psa, drug resistance research and the implementation of prevention strategies.