A putative LysR-type transcriptional regulator PrhO positively regulates the type III secretion system and contributes to the virulence of Ralstonia solanacearum
A putative LysR-type transcriptional regulator PrhO positively regulates the type III secretion system and contributes to the virulence of Ralstonia solanacearum
复制标题
假定的 LysR 型转录调节因子 PrhO 正向调节 III 型分泌系统并有助于青枯菌的毒力
DOI：
10.1111/mpp.12660
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发表时间：
2018
影响因子：
4.9
通讯作者：
Ohnishi Kouhei
中科院分区：
文献类型：
--
作者：
Zhang Yong;Li Jiaman;Zhang Weiqi;Shi Hualei;Luo Feng;Hikichi Yasufumi;Shi Xiaojun;Ohnishi Kouhei
LysR型转录调节因子（LTTR）在细菌中普遍存在且丰富，并控制各种细胞过程。本文研究了Rsc1880（一个假定的LTTR，以下简称PrhO）对青枯雷尔氏菌（Ralstonia solanacearum）致病性的影响。prhO的缺失显著降低了III型分泌系统（T3SS）在体外和植物体内的表达，并导致番茄和烟草植物中的毒力显著受损。互补的prhO完全恢复了野生型的降低的毒力和T3SS表达。此外，PrhO依赖的T3SS和毒力是保守的青枯菌物种。然而，prhO的缺失并没有改变生物膜的形成、游泳运动性和植物生长。某些III型效应子在突变体中的表达量显著降低，但对烟草的过敏反应没有影响。与HrpB对T3SS的关键调节作用一致，PrhO通过HrpB正向调节T3SS。此外，PrhO通过两个密切的旁系同源物HrpG和PrhG调节hrpB表达，这两个旁系同源物是双组分反应调节剂，并且以平行方式正向调节hrpB表达。然而，prhO的缺失并不改变同样参与hrpB调节的phcA、prhJ和prhN的表达。此外，PrhO以细胞密度依赖性方式表达，但其自身负抑制。HrpB、PhcA和PrhN对PrhO表达无调节作用。综上所述，我们从遗传学角度证明PrhO是青枯菌的一种新的毒力调节因子，它通过HrpG、PrhG和HrpB正向调节T3SS的表达，并对毒力有贡献。
LysR‐type transcriptional regulators (LTTRs) are ubiquitous and abundant amongst bacteria and control a variety of cellular processes. Here, we investigated the effect of Rsc1880 (a putative LTTR, hereafter designated as PrhO) on the pathogenicity ofRalstonia solanacearum. Deletion ofprhOsubstantially reduced the expression of the type III secretion system (T3SS) bothin vitroandin planta, and resulted in significantly impaired virulence in tomato and tobacco plants. ComplementaryprhOcompletely restored the reduced virulence and T3SS expression to that of the wild‐type. Moreover, PrhO‐dependent T3SS and virulence were conserved amongstR. solanacearumspecies. However, deletion ofprhOdid not alter biofilm formation, swimming mobility andin plantagrowth. The expression of some type III effectors was significantly reduced inprhOmutants, but the hypersensitive response was not affected in tobacco leaves. Consistent with the key regulatory role of HrpB on T3SS, PrhO positively regulated the T3SS through HrpB. Furthermore, PrhO regulatedhrpBexpression via two close paralogues, HrpG and PrhG, which are two‐component response regulators and positively regulatehrpBexpression in a parallel manner. However, deletion ofprhOdid not alter the expression ofphcA,prhJandprhN, which are also involved inhrpBregulation. In addition, PrhO was expressed in a cell density‐dependent manner, but negatively repressed by itself. No regulation was observed for HrpB, PhcA and PrhN onprhOexpression. Taken together, we genetically demonstrated that PrhO is a novel virulence regulator ofR. solanacearum, which positively regulates T3SS expression through HrpG, PrhG and HrpB and contributes to virulence.