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PMID: 7768869 Published · ppublish English Journal Article Research Support, U.S. Gov't, Non-P.H.S.

ccrA1: a mutation in Streptomyces coelicolor that affects the control of catabolite repression.

Journal of bacteriology ·Vol. 177 ·No. 12 ·1995-06-00 ·Pages 3579-86

Ingram C, Delic I, Westpheling J

Abstract

The regulation of carbon utilization is of central importance in the gene expression pathways for both morphological development and antibiotic production in Streptomyces species. We report the identification and characterization of a mutation in Streptomyces coelicolor, ccrA1, that affects the expression of several catabolite-controlled promoters. ccrA1 mutants are altered in expression of galP1, the glucose-sensitive, galactose-dependent promoter of the galactose utilization operon; in expression of the glycerol utilization operon, which is glucose sensitive and glycerol dependent; and in expression of chi63, the glucose-sensitive chitin-dependent promoter of a gene involved in chitin utilization. ccrA1 has no effect on the expression of galP2, a promoter that directs constitutive transcription of the galE and galK genes. ccrA1 maps to a region of the S. coelicolor genome which distinguishes it from other mutations known to be involved in catabolite control. We suggest that ccrA1 identifies a gene whose product may be involved in the general regulation of carbon catabolite repression in this complex bacterium.

MeSH Terms
Chromosome Mapping Crosses, Genetic Down-Regulation/genetics Gene Expression Regulation, Bacterial/genetics Mutation Operon/genetics Promoter Regions, Genetic Streptomyces/genetics,metabolism
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Ingram C
Molecular Biology Graduate Program, University of Pennsylvania, Philadelphia, USA.
Delic I
Westpheling J
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41 references, click to expand
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
Published
1995-06-00
Pages
3579-86
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC177065
Subset
IM
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