Streptomyces coelicolor produces four genetically and structurally distinct
antibiotics in a growth-phase-dependent manner. S. coelicolor mutants glob
ally deficient in antibiotic production (Abs(-) phenotype) have previously
been isolated, and some of these were found to define the absB locus. In th
is 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 def
iciency in RNase III, In marker exchange experiments, the S, coelicolor nle
gene rescued absB mutants, restoring antibiotic production. Sequencing the
DNA of absB mutants confirmed that the absB mutations lay in the me open r
eading frame. Constructed disruptions of rnc in both S. coelicolor 1501 and
Streptomyces lividans 1326 caused an Abs- phenotype, An absB mutation caus
ed 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 synth
esis of antibiotics.