THE BLD MUTANTS OF STREPTOMYCES-COELICOLOR ARE DEFECTIVE IN THE REGULATION OF CARBON UTILIZATION, MORPHOGENESIS AND CELL-CELL SIGNALING

Citation
Mk. Pope et al., THE BLD MUTANTS OF STREPTOMYCES-COELICOLOR ARE DEFECTIVE IN THE REGULATION OF CARBON UTILIZATION, MORPHOGENESIS AND CELL-CELL SIGNALING, Molecular microbiology, 19(4), 1996, pp. 747-756
Citations number
42
Categorie Soggetti
Biology,Microbiology
Journal title
ISSN journal
0950382X
Volume
19
Issue
4
Year of publication
1996
Pages
747 - 756
Database
ISI
SICI code
0950-382X(1996)19:4<747:TBMOSA>2.0.ZU;2-#
Abstract
Mutants of Streptomyces coelicolor blocked at the earliest visible sta ge of morphological differentiation are called bid mutants. These muta nts fail to form aerial hyphae on rich medium and most are defective i n antibiotic production, One striking feature of these mutants is that , with the exception of bldB, their morphological defect is carbon-sou rce dependent, In our investigation of catabolite control in Streptomy ces, we identified mutants that were resistant to glucose repression a nd were also bid, The existence of these new bld mutants led us to exa mine the catabolite control phenotype of the previously described bid mutants which were not known to contain defects in carbon regulation, We report here that all of the characterized bid mutants of S. coelico lor are defective in the regulation of galP1, and that at least one of the bid 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 bid 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 interpretat ion for the role of the bld genes in development in Streptomyces. We s uggest that the primary defect in bid 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 bid mutants to initiate morphogenesis is a secondary consequence of their inability to sense and/or signal s tarvation.