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ToxR和CalR对其自身基因及1型III型分泌系统的调控作用于…… (原文结尾不完整)

Regulatory actions of ToxR and CalR on their own genes and type III secretion system 1 in .

作者信息

Osei-Adjei George, Gao He, Zhang Ying, Zhang Lingyu, Yang Wenhui, Yang Huiying, Yin Zhe, Huang Xinxiang, Zhang Yiquan, Zhou Dongsheng

机构信息

School of Medicine, Jiangsu University, Zhenjiang 212013, China.

State Key Laboratory of Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 102206, China.

出版信息

Oncotarget. 2017 Jul 22;8(39):65809-65822. doi: 10.18632/oncotarget.19498. eCollection 2017 Sep 12.

DOI:10.18632/oncotarget.19498
PMID:29029474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5630374/
Abstract

is the leading cause of seafood-associated gastroenteritis. Type III secretion system 1 (T3SS1) is one of the virulence determinants of this bacteria. T3SS1 expression is regulated by ToxR and CalR. ToxR represses the transcription of T3SS1 genes via activation of CalR, which acts as a transcriptional repressor of T3SS1 genes. However, the transcriptional regulation mechanisms have not been elucidated. As showing in the present work, ToxR binds to the promoter DNA region of to activate its transcription. CalR occupies the promoter-proximal regions of each detected target operons in T3SS1 loci to repress their transcription, and thereby inhibiting T3SS1-dependent cytotoxicity. Moreover, a feedback CalR inhibits and its own gene in a direct manner. Collectively, this work reported an interesting gene regulatory network involving the reciprocal regulation of ToxR and CalR, and their regulation on T3SS1 genes transcription in .

摘要

是海鲜相关肠胃炎的主要病因。III型分泌系统1(T3SS1)是这种细菌的毒力决定因素之一。T3SS1的表达受ToxR和CalR调控。ToxR通过激活CalR来抑制T3SS1基因的转录,而CalR作为T3SS1基因的转录抑制因子发挥作用。然而,转录调控机制尚未阐明。如本研究所示,ToxR与 的启动子DNA区域结合以激活其转录。CalR占据T3SS1基因座中每个检测到的靶标操纵子的启动子近端区域以抑制其转录,从而抑制T3SS1依赖性细胞毒性。此外,反馈性的CalR直接抑制 及其自身基因。总的来说,这项研究报道了一个有趣的基因调控网络,涉及ToxR和CalR的相互调控,以及它们对 中T3SS1基因转录的调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/0ee1828171d0/oncotarget-08-65809-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/c5c449566e93/oncotarget-08-65809-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/84c06f2499bc/oncotarget-08-65809-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/0f29372903e1/oncotarget-08-65809-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/9d4337ac39be/oncotarget-08-65809-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/b7a412ae6007/oncotarget-08-65809-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/b539acc17a9b/oncotarget-08-65809-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/0ee1828171d0/oncotarget-08-65809-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/c5c449566e93/oncotarget-08-65809-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/84c06f2499bc/oncotarget-08-65809-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/0f29372903e1/oncotarget-08-65809-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/9d4337ac39be/oncotarget-08-65809-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/b7a412ae6007/oncotarget-08-65809-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/b539acc17a9b/oncotarget-08-65809-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e99/5630374/0ee1828171d0/oncotarget-08-65809-g007.jpg

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