Journal of Bacteriology, October 1999, p. 6142-6151, Vol. 181, No. 19
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Department of Microbiology, Michigan State University, East Lansing, Michigan 48824-1101
Received 19 April 1999/Accepted 19 July 1999
Streptomyces coelicolor produces four genetically and
structurally distinct antibiotics in a growth-phase-dependent manner. S. coelicolor mutants globally deficient in antibiotic
production (Abs
phenotype) have previously been isolated,
and some of these were found to define the absB locus. In
this study, we isolated absB-complementing DNA and show
that it encodes the S. coelicolor homolog of RNase III
(rnc). Several lines of evidence indicate that the
absB mutant global defect in antibiotic synthesis is due to
a deficiency in RNase III. In marker exchange experiments, the S. coelicolor rnc gene rescued absB mutants, restoring
antibiotic production. Sequencing the DNA of absB mutants
confirmed that the absB mutations lay in the
rnc open reading frame. Constructed disruptions of
rnc in both S. coelicolor 1501 and
Streptomyces lividans 1326 caused an Abs
phenotype. An absB mutation caused accumulation of 30S rRNA
precursors, as had previously been reported for E. coli rnc
mutants. The absB gene is widely conserved in
streptomycetes. We speculate on why an RNase III deficiency could
globally affect the synthesis of antibiotics.
Present address: Abbott Laboratories, Abott Park, Ill.
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 |