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毒力质粒pXO1的Rap磷酸酶抑制炭疽芽孢杆菌的孢子形成。

Rap phosphatase of virulence plasmid pXO1 inhibits Bacillus anthracis sporulation.

作者信息

Bongiorni Cristina, Stoessel Ricarda, Shoemaker Dorinda, Perego Marta

机构信息

Division of Cellular Biology, Mail Code: MEM-116, Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037.

出版信息

J Bacteriol. 2006 Jan;188(2):487-98. doi: 10.1128/JB.188.2.487-498.2006.

Abstract

This study shows that the Bacillus anthracis pXO1 virulence plasmid carries a Rap-Phr system, BXA0205, which regulates sporulation initiation in this organism. The BXA0205Rap protein was shown to dephosphorylate the Spo0F response regulator intermediate of the phosphorelay signal transduction system that regulates the initiation of the developmental pathway in response to environmental, metabolic, and cell cycle signals. The activity of the Rap protein was shown to be inhibited by the carboxy-terminal pentapeptide generated through an export-import processing pathway from the associated BXA0205Phr protein. Deregulation of the Rap activity by either overexpression or lack of the Phr pentapeptide resulted in severe inhibition of sporulation. Five additional Rap-Phr encoding systems were identified on the chromosome of B. anthracis, one of which, BA3790-3791, also affected sporulation initiation. The results suggest that the plasmid-borne Rap-Phr system may provide a selective advantage to the virulence of B. anthracis.

摘要

本研究表明,炭疽芽孢杆菌pXO1毒力质粒携带一个Rap-Phr系统BXA0205,该系统调节该生物体中的芽孢形成起始。已证明BXA0205Rap蛋白可使磷中继信号转导系统的Spo0F应答调节中间体去磷酸化,该系统响应环境、代谢和细胞周期信号调节发育途径的起始。已证明Rap蛋白的活性受到通过相关BXA0205Phr蛋白的输出-输入加工途径产生的羧基末端五肽的抑制。通过过表达或缺乏Phr五肽使Rap活性失调会导致芽孢形成受到严重抑制。在炭疽芽孢杆菌染色体上鉴定出另外五个编码Rap-Phr的系统,其中一个BA3790-3791也影响芽孢形成起始。结果表明,质粒携带的Rap-Phr系统可能为炭疽芽孢杆菌的毒力提供选择优势。

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