Abstract
Escherichia coli RecX (RecX(Ec)) is a negative regulator of RecA activities both in the bacterial cell and in vitro. In contrast, the Neisseria gonorrhoeae RecX protein (RecX(Ng)) enhances all RecA-related processes in N. gonorrhoeae. Surprisingly, the RecX(Ng) protein is not a RecA protein activator in vitro. Instead, RecX(Ng) is a much more potent inhibitor of all RecA(Ng) and RecA(Ec) activities than is the E. coli RecX ortholog. A series of RecX(Ng) mutant proteins representing a gradient of functional deficiencies provide a direct correlation between RecA(Ng) inhibition in vitro and the enhancement of RecA(Ng) function in N. gonorrhoeae. Unlike RecX(Ec), 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 RecX(Ng) protein-mediated limitations on RecA(Ng) filament presence and/or length to achieve maximal function.
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