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LexA cleavage is required for CTX prophage induction
Mariam Quinones1, Harvey H Kimsey, Matthew K Waldor
1Department of Molecular Microbiology, Tufts University School of Medicine and The Howard Hughes Medical Institute, Boston, MA 02111, USA.
Molecular Cell
|January 25, 2005
Summary
The Vibrio cholerae SOS response regulates cholera toxin phage (CTXphi) production by controlling the repressor LexA. UV radiation triggers RecA-dependent LexA cleavage, activating CTXphi. This reveals a novel phage regulation mechanism.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Temperate phage production mechanisms are poorly understood.
- CTXphi is a temperate filamentous phage infecting Vibrio cholerae, encoding cholera toxin.
- CTXphi lysogens involve repressor RstR controlling the P(rstA) promoter.
Purpose of the Study:
- Investigate CTXphi production regulation in Vibrio cholerae.
- Elucidate the role of the SOS response in CTXphi production.
- Compare CTXphi SOS regulation to other prophages.
Main Methods:
- Studied CTXphi production in Vibrio cholerae lysogens.
- Investigated the impact of UV radiation on CTXphi production.
- Analyzed the roles of RecA and LexA in CTXphi regulation.
Main Results:
- The Vibrio cholerae SOS response regulates CTXphi production.
- UV-stimulated CTXphi production depends on RecA-mediated LexA autocleavage.
- Both LexA and RstR repress the CTXphi P(rstA) promoter.
Conclusions:
- CTXphi production is controlled by a repressor (LexA) regulated by the SOS response to DNA damage.
- This mechanism differs from SOS-mediated prophage induction in E. coli.
- The findings provide new insights into temperate phage regulation.