Journal of Bacteriology, July 1999, p. 4266-4274, Vol. 181, No. 14
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


Division of Infectious Diseases, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115
Received 10 September 1998/Accepted 5 May 1999
Extracytoplasmic function (ECF) sigma factors are a heterogeneous
group of alternative sigma factors that regulate gene expression in
response to a variety of conditions, including stress. We previously characterized a mycobacterial ECF sigma factor, SigE, that contributes to survival following several distinct stresses. A gene encoding a
closely related sigma factor, sigH, was cloned from
Mycobacterium tuberculosis and Mycobacterium
smegmatis. A single copy of this gene is present in these and
other fast- and slow-growing mycobacteria, including M. fortuitum and M. avium. While the M. tuberculosis and M. smegmatis sigH genes encode
highly similar proteins, there are multiple differences in adjacent
genes. The single in vivo transcriptional start site identified in
M. smegmatis and one of two identified in M. bovis BCG were found to have
35 promoter sequences that match
the ECF-dependent
35 promoter consensus. Expression from these
promoters was strongly induced by 50°C heat shock. In comparison to
the wild type, an M. smegmatis sigH mutant was found to be
more susceptible to cumene hydroperoxide stress but to be similar in
logarithmic growth, stationary-phase survival, and survival following
several other stresses. Survival of an M. smegmatis sigH
sigE double mutant was found to be markedly decreased following
53°C heat shock and following exposure to cumene hydroperoxide.
Expression of the second gene in the sigH operon is
required for complementation of the sigH stress phenotypes. SigH is an alternative sigma factor that plays a role in the
mycobacterial stress response.
Present address: Dyax Corporation, Cambridge, MA 02139.
Present address: Department of Cardiology, Brigham and Women's
Hospital, Boston, MA 02115.
This article has been cited by other articles:
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
| ALL ASM JOURNALS |