Identification of a putative cognate sensor kinase for the two-component response regulator HrpG, a key regulator controlling the expression of the hrp genes in Xanthomonas campestris pv. campestris
Identification of a putative cognate sensor kinase for the two-component response regulator HrpG, a key regulator controlling the expression of the hrp genes in Xanthomonas campestris pv. campestris
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DOI：
10.1111/1462-2920.12207
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发表时间：
2014-07-01
影响因子：
5.1
通讯作者：
Tang, Ji-Liang
中科院分区：
文献类型：
--
作者：
Li, Rui-Fang;Lu, Guang-Tao;Tang, Ji-Liang
植物致病菌油菜黄单胞菌pv。campestris （Xcc）依靠hrp （hypersensitive response and致病性）基因引起疾病并诱导hypersensitive response （HR）。细菌性植物病原体的hrp基因分为两组。Xcc hrp基因属于II组。人们早就知道，II组hrp基因是由一种arac型转录调控因子激活的，这种转录调控因子的表达受一种双组分系统（TCS）反应调控因子（在Xcc中称为HrpG）的控制。然而，尚未发现同源的传感器激酶。在这里，我们提供的证据表明Xcc开放阅读框XC_3670编码TCS传感器激酶（称为HpaS）。hpaS突变几乎完全消除了HR诱导和毒力。细菌双杂交和蛋白下拉实验显示，HpaS与HrpG发生物理相互作用。Phos-tag (TM) SDS-PAGE分析显示，hpaS突变显著降低了体内HrpG的磷酸化水平。这些数据表明HpaS和HrpG最有可能形成TCS。我们还发现XC_3669（命名为hpaR2）与hpaS相邻，编码一个假定的TCS反应调节因子，是完全毒力所必需的，但不是HR诱导所必需的。HpaR2也与HpaS发生物理相互作用，表明HpaS也可能与HpaR2形成另一种TCS。
The bacterial phytopathogen Xanthomonas campestris pv. campestris (Xcc) relies on the hrp (hypersensitive response and pathogenicity) genes to cause disease and induce hypersensitive response (HR). The hrp genes of bacterial phytopathogens are divided into two groups. Xcc hrp genes belong to group II. It has long been known that the group II hrp genes are activated by an AraC-type transcriptional regulator whose expression is controlled by a two-component system (TCS) response regulator (named HrpG in Xcc). However, no cognate sensor kinase has yet been identified. Here, we present evidence showing that the Xcc open-reading frame XC_3670 encodes a TCS sensor kinase (named HpaS). Mutation of hpaS almost completely abolished the HR induction and virulence. Bacterial two-hybrid and protein pull-down assays revealed that HpaS physically interacted with HrpG. Phos-tag (TM) SDS-PAGE analysis showed that mutation in hpaS reduced markedly the phosphorylation of HrpG in vivo. These data suggest that HpaS and HrpG are most likely to form a TCS. We also showed that XC_3669 (named hpaR2), which is adjacent to hpaS and encodes a putative TCS response regulator, is required for full virulence but not HR induction. HpaR2 also physically interacted with HpaS, suggesting that HpaS may also form another TCS with HpaR2.