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Journal of Bacteriology, April 2004, p. 1999-2005, Vol. 186, No. 7
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.7.1999-2005.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Sporulation Phenotype of a Bacillus subtilis Mutant Expressing an Unprocessable but Active {sigma}E Transcription Factor

Shonna McBride and W. G. Haldenwang*

Department of Microbiology and Immunology, University of Texas Health Science Center, San Antonio, Texas 78229-3900

Received 6 October 2003/ Accepted 22 December 2003

{sigma}E, a sporulation-specific sigma factor of Bacillus subtilis, is formed from an inactive precursor (pro-{sigma}E) by a developmentally regulated processing reaction that removes 27 amino acids from the proprotein's amino terminus. A sigE variant (sigE335) lacking 15 amino acids of the prosequence is not processed into mature {sigma}E but is active without processing. In the present work, we investigated the sporulation defect in sigE335-expressing B. subtilis, asking whether it is the bypass of proprotein processing or a residual inhibition of {sigma}E activity that is responsible. Fluorescence microscopy demonstrated that sigE335-expressing B. subtilis progresses further into sporulation (stage III) than do strains lacking {sigma}E activity (stage II). Consistent with its stage III phenotype, and a defect in {sigma}E activity rather than its timing, the sigE335 allele did not disturb early sporulation gene expression but did inhibit the expression of late sporulation genes (gerE and sspE). The Spo- phenotype of sigE335 was found to be recessive to wild-type sigE. In vivo assays of {sigma}E activity in sigE, sigE335, and merodiploid strains indicate that the residual prosequence on {sigma}E335, still impairs its activity to function as a transcription factor. The data suggest that the 11-amino-acid extension on {sigma}E335 allows it to bind RNA polymerase and direct the resulting holoenzyme to {sigma}E-dependent promoters but reduces the enzyme's ability to initiate transcription initiation and/or exit from the promoter.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, MSC-7758, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229-3900. Phone: (210) 567-3957. Fax: (210) 567-6612. E-mail: Haldenwang{at}uthscsa.edu.

Journal of Bacteriology, April 2004, p. 1999-2005, Vol. 186, No. 7
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.7.1999-2005.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.





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