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PrhN是一种假定的marR家族转录调节因子,参与III型分泌系统的正调控以及青枯雷尔氏菌的完全毒力。

PrhN, a putative marR family transcriptional regulator, is involved in positive regulation of type III secretion system and full virulence of Ralstonia solanacearum.

作者信息

Zhang Yong, Luo Feng, Wu Dousheng, Hikichi Yasufumi, Kiba Akinori, Igarashi Yasuo, Ding Wei, Ohnishi Kouhei

机构信息

Research Center of Bioenergy and Bioremediation, Southwest University Chongqing, China.

College of Plant Protection, Southwest University Chongqing, China.

出版信息

Front Microbiol. 2015 Apr 28;6:357. doi: 10.3389/fmicb.2015.00357. eCollection 2015.

DOI:10.3389/fmicb.2015.00357
PMID:25972849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4412082/
Abstract

The MarR-family of transcriptional regulators are involved in various cellular processes, including resistance to multiple antibiotics and other toxic chemicals, adaptation to different environments and pathogenesis in many plant and animal pathogens. Here, we reported a new MarR regulator PrhN, which was involved in the pathogenesis of Ralstonia solanacearum. prhN mutant exhibited significantly reduced virulence and stem colonization compared to that of wild type in tomato plants. prhN mutant caused identical hypersensitive response (HR) on resistant plants to the wild type. Deletion of prhN gene substantially reduced the expression of type III secretion system (T3SS) in vitro and in planta (mainly in tomato plants), which is essential for pathogenicity of R. solanacearum, and the complemented PrhN could restore its virulence and T3SS expression to that of wild type. T3SS is directly controlled by AraC-type transcriptional regulator HrpB, and the transcription of hrpB is activated by HrpG and PrhG. HrpG and PrhG are homologs but are regulated by the PhcA positively and negatively, respectively. Deletion of prhN gene also abolished the expression of hrpB and prhG, but didn't change the expression of hrpG and phcA. Together, these results indicated that PrhN positively regulates T3SS expression through PrhG and HrpB. PrhN and PhcA should regulate prhG expression in a parallel way. This is the first report on the pathogenesis of MarR regulator in R. solanacearum, and this new finding will improve our understanding on the various biological functions of MarR regulator and the complex regulatory network on hrp regulon in R. solanacearum.

摘要

转录调节因子的MarR家族参与多种细胞过程,包括对多种抗生素和其他有毒化学物质的抗性、适应不同环境以及许多动植物病原体的致病过程。在此,我们报道了一种新的MarR调节因子PrhN,它参与了青枯雷尔氏菌的致病过程。与野生型相比,prhN突变体在番茄植株中的毒力和茎部定殖能力显著降低。prhN突变体在抗性植株上引起的过敏反应(HR)与野生型相同。prhN基因的缺失在体外和体内(主要在番茄植株中)显著降低了III型分泌系统(T3SS)的表达,而T3SS对青枯雷尔氏菌的致病性至关重要,互补的PrhN可以将其毒力和T3SS表达恢复到野生型水平。T3SS直接受AraC型转录调节因子HrpB控制,hrpB的转录由HrpG和PrhG激活。HrpG和PrhG是同源物,但分别受到PhcA的正向和负向调节。prhN基因的缺失也消除了hrpB和prhG的表达,但没有改变hrpG和phcA的表达。总之,这些结果表明PrhN通过PrhG和HrpB正向调节T3SS的表达。PrhN和PhcA应该以平行的方式调节prhG的表达。这是关于MarR调节因子在青枯雷尔氏菌致病机制方面的首次报道,这一新发现将增进我们对MarR调节因子的各种生物学功能以及青枯雷尔氏菌中hrp操纵子复杂调控网络的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/ea02bfe3144b/fmicb-06-00357-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/e64f6c706793/fmicb-06-00357-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/77ba0da92b0a/fmicb-06-00357-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/bf02ebabe4e7/fmicb-06-00357-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/2a621d5a0079/fmicb-06-00357-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/2596bb114019/fmicb-06-00357-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/10b03aa41060/fmicb-06-00357-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/ea02bfe3144b/fmicb-06-00357-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/e64f6c706793/fmicb-06-00357-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/77ba0da92b0a/fmicb-06-00357-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/bf02ebabe4e7/fmicb-06-00357-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/2a621d5a0079/fmicb-06-00357-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/2596bb114019/fmicb-06-00357-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/10b03aa41060/fmicb-06-00357-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddd9/4412082/ea02bfe3144b/fmicb-06-00357-g0007.jpg

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