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Journal of Bacteriology, October 2005, p. 6832-6840, Vol. 187, No. 19
0021-9193/05/$08.00+0     doi:10.1128/JB.187.19.6832-6840.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Control of the Expression and Compartmentalization of {sigma}G Activity during Sporulation of Bacillus subtilis by Regulators of {sigma}F and {sigma}E

Vasant K. Chary, Mauro Meloni,{dagger} David W. Hilbert,{ddagger} and Patrick J. Piggot*

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania

Received 10 June 2005/ Accepted 22 July 2005

During formation of spores by Bacillus subtilis the RNA polymerase factor {sigma}G ordinarily becomes active during spore formation exclusively in the prespore upon completion of engulfment of the prespore by the mother cell. Formation and activation of {sigma}G ordinarily requires prior activity of {sigma}F in the prespore and {sigma}E in the mother cell. Here we report that in spoIIA mutants lacking both {sigma}F and the anti-sigma factor SpoIIAB and in which {sigma}E is not active, {sigma}G nevertheless becomes active. Further, its activity is largely confined to the mother cell. Thus, there is a switch in the location of {sigma}G activity from prespore to mother cell. Factors contributing to the mother cell location are inferred to be read-through of spoIIIG, the structural gene for {sigma}G, from the upstream spoIIG locus and the absence of SpoIIAB, which can act in the mother cell as an anti-sigma factor to {sigma}G. When the spoIIIG locus was moved away from spoIIG to the distal amyE locus, {sigma}G became active earlier in sporulation in spoIIA deletion mutants, and the sporulation septum was not formed, suggesting that premature {sigma}G activation can block septum formation. We report a previously unrecognized control in which SpoIIGA can prevent the appearance of {sigma}G activity, and pro-{sigma}E (but not {sigma}E) can counteract this effect of SpoIIGA. We find that in strains lacking {sigma}F and SpoIIAB and engineered to produce active {sigma}E in the mother cell without the need for SpoIIGA, {sigma}G also becomes active in the mother cell.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, 3400 North Broad Street, Philadelphia, PA 19140. Phone: (215) 707-7927. Fax: (215) 707-7788. E-mail: piggotp{at}temple.edu.

{dagger} Present address: Unité des Toxins et Pathogénie Bactérienne, Institut Pasteur, 75724 Paris Cedex 15, France.

{ddagger} Present address: Department of Anatomy and Cell Biology, Columbia University, New York, NY 10032.


Journal of Bacteriology, October 2005, p. 6832-6840, Vol. 187, No. 19
0021-9193/05/$08.00+0     doi:10.1128/JB.187.19.6832-6840.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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