The bld mutants of Streptomyces coelicolor are defective in the regulation of carbon utilization, morphogenesis and cell–cell signalling
Authors: Pope, Margaret K.; Green, Brian D.; Westpheling, Janet
Source: Molecular Microbiology, Volume 19, Number 4, February 1996 , pp. 747-756(10)
Abstract:Mutants of Streptomyces coelicolor blocked at the earliest visible stage of morphological differentiation are called bld mutants. These mutants fail to form aerial hyphae on rich medium and most are defective in antibiotic production. One striking feature of these mutants is that, with the exception of bldB, their morphological defect is carbon-source dependent. In our investigation of catabolite control in Streptomyces, we identified mutants that were resistant to glucose repression and were also bld. The existence of these new bld mutants led us to examine the catabolite control phenotype of the previously described bld mutants which were not known to contain defects in carbon regulation. We report here that all of the characterized bld mutants of S.coelicolor are defective in the regulation of galP1, and that at least one of the bld mutants, bldB, is globally deregulated for carbon utilization. Complementation of the morphological defect of bldA and bldB mutants with a cloned copy of the wild-type bld gene simultaneously restored normal regulation of galP1, indicating that both aspects of the mutant phenotype are caused by the same lesion. We suggest a new interpretation for the role of the bld genes in development in Streptomyces. We suggest that the primary defect in bld mutants is in the regulation of carbon utilization, not specifically in the activation of genes whose products regulate the development pathway as previously suggested. We speculate that the inability of bld mutants to initiate morphogenesis is a secondary consequence of their inability to sense and/or signal starvation.
Document Type: Research Article
Affiliations: University of Georgia, Genetics Department, Athens, Georgia 30602, USA
Publication date: February 1, 1996