Rot and Agr system modulate fibrinogen-binding ability mainly by regulating clfB expression in Staphylococcus aureus NCTC8325
Rot and Agr system modulate fibrinogen-binding ability mainly by regulating clfB expression in Staphylococcus aureus NCTC8325
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Rot和Agr系统主要通过调节金黄色葡萄球菌NCTC8325中clfB的表达来调节纤维蛋白原结合能力
DOI：
10.1007/s00430-011-0208-z
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发表时间：
2011-06
影响因子：
5.4
通讯作者：
Sun, Baolin
中科院分区：
文献类型：
--
作者：
Xue, Ting;You, Yibo;Shang, Fei;Sun, Baolin
金黄色葡萄球菌是一种重要的人类病原体，可引起多种疾病，从局部皮肤感染到危及生命的全身感染。金黄色葡萄球菌作为病原体的成功部分归因于其通过与宿主细胞外基质蛋白（如纤维蛋白原、纤连蛋白和胶原蛋白）结合而粘附于多种宿主组织的能力。金黄色葡萄球菌表达两种可以特异性结合纤维蛋白原的蛋白质，即凝集因子 A 和 B（ClfA 和 ClfB）。已知毒素阻遏蛋白 (Rot) 是金黄色葡萄球菌毒力基因表达的全局调节因子。 Rot 的翻译受到葡萄球菌辅助基因调节器 (Agr) 群体感应系统的调节。在本研究中，我们证明了金黄色葡萄球菌NCTC8325中的Rot和Agr系统可以在不同细菌生长阶段影响细菌与人纤维蛋白原（Fg）的结合能力。我们的实时 RT-PCR 结果表明 Rot 和 Agr 系统对 clfA 表达没有显着影响。然而，Rot是clfB的激活剂，Agr/RNAIII可以通过Rot调节clfB的表达。凝胶位移数据进一步表明 Rot 可能通过直接结合 clfB 的启动子区域来调节 clfB 表达。此外，Rot和Agr系统对clfB转录和细菌Fg结合能力表现出一致的调节作用，表明Rot和Agr系统可能主要通过调节clfB转录来影响细菌Fg结合能力。
Staphylococcus aureus is an important human pathogen that causes a variety of diseases, ranging from localized skin infections to life-threatening systemic infections. The success of S. aureus as a pathogen is partly due to its ability to adhere to a wide range of host tissues by binding to host extracellular matrix proteins such as fibrinogen, fibronectin, and collagen. Staphylococcus aureus expresses two proteins that can bind specifically to fibrinogen, clumping factors A and B (ClfA and ClfB). Repressor of toxins (Rot) is known to be a global regulator of virulence gene expression in S. aureus. The translation of Rot is regulated by the staphylococcal accessory gene regulator (Agr) quorum-sensing system. In this study, we demonstrated that Rot and the Agr system in S. aureus NCTC8325 can affect the bacterial binding ability to human fibrinogen (Fg) under different bacterial growth phases. Our real-time RT-PCR results indicated that both Rot and the Agr system have no significant effect on clfA expression. However, Rot is an activator of clfB, and Agr/RNAIII can regulate clfB expression via Rot. Gel shift data further suggested that Rot might regulate clfB expression by directly binding to the promoter region of clfB. Moreover, Rot and the Agr system exhibited consistent regulatory effects on clfB transcription and bacterial Fg-binding ability, suggesting that Rot and the Agr system might affect bacterial Fg-binding ability mainly through regulating clfB transcription.
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影响因子：
4.8
作者：
McAleese, FM;Walsh, EJ;Foster, TJ
通讯作者：
Foster, TJ
影响因子：
3.6
作者：
Ni Eidhin, Deirdre;Perkins, Samuel;Foster, Timothy J.
通讯作者：
Foster, Timothy J.
DOI：
10.1161/01.atv.0000237606.90253.94
发表时间：
2006-10
期刊：
Arteriosclerosis, Thrombosis, and Vascular Biology
影响因子：
--
作者：
Niraj Procopio Evagrio George;Q. Wei;P. Shin;K. Konstantopoulos;J. Ross
通讯作者：
Niraj Procopio Evagrio George;Q. Wei;P. Shin;K. Konstantopoulos;J. Ross
影响因子：
3.6
作者：
MCDEVITT, D;FRANCOIS, P;FOSTER, TJ
通讯作者：
FOSTER, TJ
影响因子：
3.1
作者：
McNamara, PJ;Bayer, AS
通讯作者：
Bayer, AS