Abstract
Escherichia coli RecX (RecXEc) is a negative regulator of RecA activities both in the bacterial cell and in vitro. In contrast, the Neisseria gonorrhoeae RecX protein (RecXNg) enhances all RecA-related processes in N. gonorrhoeae. Surprisingly, the RecXNg protein is not a RecA protein activator in vitro. Instead, RecXNg is a much more potent inhibitor of all RecANg and RecAEc activities than is the E. coli RecX ortholog. A series of RecXNg mutant proteins representing a gradient of functional deficiencies provide a direct correlation between RecANg inhibition in vitro and the enhancement of RecA Ng function in N. gonorrhoeae. Unlike RecXEc, RecX Ng does not simply cap the growing ends of RecA filaments, but it directly facilitates a more rapid RecA filament disassembly. Thus, in N. gonorrhoeae, recombinational processes are facilitated by RecXNg protein-mediated limitations on RecANg filament presence and/or length to achieve maximal function. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
Cite
CITATION STYLE
Gruenig, M. C., Stohl, E. A., Chitteni-Pattu, S., Seifert, H. S., & Cox, M. M. (2010). Less is more: Neisseria gonorrhoeae RecX protein stimulates recombination by inhibiting RecA. Journal of Biological Chemistry, 285(48), 37188–37197. https://doi.org/10.1074/jbc.M110.171967
Register to see more suggestions
Mendeley helps you to discover research relevant for your work.