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Journal of Bacteriology, May 1999, p. 2883-2888, Vol. 181, No. 9
Department of Microbiology, Boston University
School of Medicine, Boston, Massachusetts 02118
Received 1 December 1998/Accepted 1 March 1999
In Bacillus subtilis, CcpA-dependent carbon catabolite
repression (CCR) mediated at several cis-acting
carbon repression elements (cre) requires the
seryl-phosphorylated form of both the HPr (ptsH) and Crh
(crh) proteins. During growth in minimal medium, the
ptsH1 mutation, which prevents seryl phosphorylation of
HPr, partially relieves CCR of several genes regulated by CCR.
Examination of the CCR of the histidine utilization (hut)
enzymes in cells grown in minimal medium showed that neither the
ptsH1 nor the crh mutation individually
had any affect on hut CCR but that hut CCR was
abolished in a ptsH1 crh double mutant. In contrast, the
ptsH1 mutation completely relieved hut CCR in
cells grown in Luria-Bertani medium. The ptsH1 crh double
mutant exhibited several growth defects in glucose minimal medium,
including reduced rates of growth and growth inhibition by high levels
of glycerol or histidine. CCR is partially relieved in B. subtilis mutants which synthesize low levels of active glutamine
synthetase (glnA). In addition, these glnA
mutants grow more slowly than wild-type cells in glucose minimal
medium. The defects in growth and CCR seen in these mutants are
suppressed by mutational inactivation of TnrA, a global nitrogen regulatory protein. The inappropriate expression of TnrA-regulated genes in this class of glnA mutants may deplete
intracellular pools of carbon metabolites and thereby result in the
reduction of the growth rate and partial relief of CCR.
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
trans-Acting Factors Affecting Carbon
Catabolite Repression of the hut Operon in
Bacillus subtilis
*
Corresponding author. Mailing address: Department of
Microbiology, Boston University School of Medicine, 715 Albany St.,
Boston, MA 02118. Phone: (617) 638-5498. Fax: (617) 638-4286. E-mail: shfisher{at}bu.edu.
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