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J. Bacteriol., Jun 1996, 3221-3231, Vol 178, No. 11
P Brian, PJ Riggle, RA Santos and WC Champness
Streptomycete antibiotic synthesis is coupled to morphological
differentiation such that antibiotics are produced as a colony sporulates.
Streptomyces coelicolor produces several structurally and genetically
distinct antibiotics. The S. coelicolor absA locus was defined by four
UV-induced mutations that globally blocked antibiotic biosynthesis without
blocking morphological differentiation. We show that the absA locus encodes
a putative eubacterial two-component sensor kinase-response regulator
system. All four mutations lie within a single open reading frame,
designated absA1, which is predicted to encode a sensor histidine kinase. A
second gene downstream of absA1, absA2, is predicted to encode the cognate
response regulator. In marked contrast to the antibiotic-deficient
phenotype of the previously described absA mutants, the phenotype caused by
disruption mutations in the absA locus is precocious hyperproduction of the
antibiotics actinorhodin and undecylprodigiosin. Precocious hyperproduction
of these antibiotics is correlated with premature expression of XylE
activity in a transcriptional fusion to an actinorhodin biosynthetic gene.
We propose that the absA locus encodes a signal transduction mechanism that
negatively regulates synthesis of the multiple antibiotics produced by S.
coelicolor.
Copyright © 1996, American Society for Microbiology
Global negative regulation of Streptomyces coelicolor antibiotic synthesis mediated by an absA-encoded putative signal transduction system
Department of Microbiology, Michigan State University, East Lansing, 48824-1101, USA.
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