Regulation of the co-evolved HrpR and HrpS AAA+ proteins required for Pseudomonas syringae pathogenicity.
Regulation of the co-evolved HrpR and HrpS AAA+ proteins required for Pseudomonas syringae pathogenicity.
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DOI：
10.1038/ncomms1177
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发表时间：
2011-02-01
影响因子：
16.6
通讯作者：
Schumacher J
中科院分区：
文献类型：
--
作者：
Jovanovic M;James EH;Burrows PC;Rego FG;Buck M;Schumacher J
细菌的AAA+增强子结合蛋白（EBP）HrpR和HrpS（HrpRS）在hrpL启动子激活σ54依赖性转录;触发3型分泌系统介导的致病性。与单独作用的EBP相比，严格合作的HrpRS对的进化提出了这个转录控制系统提供的潜在益处和机制差异的问题。在这里，我们显示了不同的属性HrpR和HrpS的变体，表明这些非冗余的，串联排列的旁系同源物的功能专业化。对Pspv. HrpR、HrpS及其控制蛋白HrpV和HrpG的活性进行了研究。番茄DC 3000体外培养证实了HrpRS形成转录活性的异源六聚体，HrpV通过特异性结合HrpS具有直接的负调节作用，HrpG抑制HrpV。不同的HrpR和HrpS功能性表明部分parkingdegeneration如何潜在地导致EBP的新控制机制，并表明EBP在σ54-RNA聚合酶活化中的亚基特异性作用。 假单胞菌的HrpR和HrpS增强子结合蛋白激活HrpL启动子的σ54依赖性转录，并且是3型分泌致病性所需的。在这里，作者证明，尽管受到共调节，但HrpR和HrpS各自具有激活σ54的不同功能。
The bacterial AAA+ enhancer-binding proteins (EBPs) HrpR and HrpS (HrpRS) of Pseudomonas syringae (Ps) activate σ54-dependent transcription at the hrpL promoter; triggering type-three secretion system-mediated pathogenicity. In contrast with singly acting EBPs, the evolution of the strictly co-operative HrpRS pair raises questions of potential benefits and mechanistic differences this transcription control system offers. Here, we show distinct properties of HrpR and HrpS variants, indicating functional specialization of these non-redundant, tandemly arranged paralogues. Activities of HrpR, HrpS and their control proteins HrpV and HrpG from Ps pv. tomato DC3000 in vitro establish that HrpRS forms a transcriptionally active hetero-hexamer, that there is a direct negative regulatory role for HrpV through specific binding to HrpS and that HrpG suppresses HrpV. The distinct HrpR and HrpS functionalities suggest how partial paralogue degeneration has potentially led to a novel control mechanism for EBPs and indicate subunit-specific roles for EBPs in σ54-RNA polymerase activation. HrpR and HrpS enhancer-binding proteins of Pseudomonas syringae activate σ54-dependent transcription of the HrpL promoter and are required for type-three secretion pathogenicity. Here, the authors demonstrate that, despite being co-regulated, HrpR and HrpS each have distinct functions for activating σ54.