A cloned regulatory gene of Streptomyces lividans can suppress the pigment deficiency phenotype of different developmental mutants.
We report here the cloning of a Streptomyces lividans gene that when introduced on a multicopy plasmid vector reversed the pigment deficiency phenotype of several distinct mutants blocked in development, pigment production, or both. Although this gene was shown by restriction enzyme analysis to be similar to a previously cloned afsB-complementing gene of Streptomyces coelicolor, we show that it does not correspond to the S. coelicolor chromosomal locus designated afsB. Thus, the cloned locus, which we propose to rename afsR, appears to complement the AfsB- phenotype by pleiotropic regulatory effects.
Stein
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Department of Genetics, Stanford University School of Medicine, California 94305.
Cohen
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D015139:Blotting, Southern; D003001:Cloning, Molecular; D005786:Gene Expression Regulation; D005798:Genes, Bacterial; D005809:Genes, Regulator; D010858:Pigmentation; D015183:Restriction Mapping; D013302:Streptomyces / Q000235:genetics*; D013489:Suppression, Genetic