Table_8_Complete Genome Sequence Analysis of Ralstonia solanacearum Strain PeaFJ1 Provides Insights Into Its Strong Virulence in Peanut Plants.XLS

The bacterial wilt of peanut (Arachis hypogaea L.) caused by Ralstonia solanacearum is a devastating soil-borne disease that seriously restricted the world peanut production. However, the molecular mechanism of R. solanacearum–peanut interaction remains largely unknown. We found that R. solanacearum HA4-1 and PeaFJ1 isolated from peanut plants showed different pathogenicity by inoculating more than 110 cultivated peanuts. Phylogenetic tree analysis demonstrated that HA4-1 and PeaFJ1 both belonged to phylotype I and sequevar 14M, which indicates a high degree of genomic homology between them. Genomic sequencing and comparative genomic analysis of PeaFJ1 revealed 153 strain-specific genes compared with HA4-1. The PeaFJ1 strain-specific genes consisted of diverse virulence-related genes including LysR-type transcriptional regulators, two-component system-related genes, and genes contributing to motility and adhesion. In addition, the repertoire of the type III effectors of PeaFJ1 was bioinformatically compared with that of HA4-1 to find the candidate effectors responsible for their different virulences. There are 79 effectors in the PeaFJ1 genome, only 4 of which are different effectors compared with HA4-1, including RipS4, RipBB, RipBS, and RS_T3E_Hyp6. Based on the virulence profiles of the two strains against peanuts, we speculated that RipS4 and RipBB are candidate virulence effectors in PeaFJ1 while RipBS and RS_T3E_Hyp6 are avirulence effectors in HA4-1. In general, our research greatly reduced the scope of virulence-related genes and made it easier to find out the candidates that caused the difference in pathogenicity between the two strains. These results will help to reveal the molecular mechanism of peanut–R. solanacearum interaction and develop targeted control strategies in the future.

由青枯雷尔氏菌（Ralstonia solanacearum）引发的花生（Arachis hypogaea L.）青枯病是一种毁灭性土传病害，严重制约全球花生产业发展。然而，青枯雷尔氏菌与花生互作的分子机制目前仍知之甚少。本研究通过对110余份栽培花生开展接种实验，发现从花生植株中分离得到的青枯雷尔氏菌HA4-1与PeaFJ1菌株致病力存在显著差异。系统发育树分析表明，HA4-1与PeaFJ1均归属于进化群I（phylotype I）和序列变种14M（sequevar 14M），提示二者基因组同源性极高。对PeaFJ1进行基因组测序与比较基因组分析后发现，相较于HA4-1，PeaFJ1含有153个菌株特异性基因，这些基因涵盖了多种毒力相关功能类群，包括LysR型转录调节因子（LysR-type transcriptional regulators）、双组分系统（two-component system）相关基因，以及参与运动性与黏附过程的基因。此外，本研究通过生物信息学手段比对PeaFJ1与HA4-1的III型效应子（type III effectors）谱，以筛选导致二者致病力差异的候选效应子。结果显示，PeaFJ1基因组共编码79个效应子，其中仅4个与HA4-1存在差异，分别为RipS4、RipBB、RipBS及RS_T3E_Hyp6。基于两菌株对花生的致病力表型，我们推测RipS4与RipBB为PeaFJ1中的候选毒力效应子，而RipBS与RS_T3E_Hyp6则是HA4-1中的无毒效应子。综上，本研究大幅缩小了毒力相关基因的筛选范围，更便于识别导致两菌株致病力差异的候选基因。上述结果有助于揭示花生与青枯雷尔氏菌互作的分子机制，并为未来开发针对性防控策略提供理论支撑。