A new GntR family transcriptional regulator in streptomyces coelicolor is required for morphogenesis and antibiotic production and controls transcription of an ABC transporter in response to carbon source.
We recently reported the isolation and initial characterization of a transposon-generated mutation that resulted in defects in both morphogenesis and antibiotic production in Streptomyces coelicolor. The insertion identified the SCO7168 open reading frame whose predicted product is a GntR family transcriptional regulator. Here, we show that this gene acts to repress transcription of itself as well as a series of genes immediately adjacent to it on the S. coelicolor chromosome that likely encode an ATP-binding cassette (ABC)-type transporter for carbohydrate uptake. Transcription of this transporter is strongly induced by growth on relatively poor carbon sources such as trehalose and melibiose and weakly induced by lactose and glycerol but not glucose, and induction is not repressed by the presence of glucose. Constructed deletions of the ABC transporter itself resulted in the suppression of the original transposon mutation, suggesting that inappropriate expression of the ABC transporter is responsible, at least in part, for the mutant phenotype. Because this transporter responds to the presence of alpha-glucosides and has similarity to two other carbohydrate transporters of this class, we have named the genes of the transporter agl3E, agl3F, and agl3G and the GntR-like protein that regulates transcription of the transporter agl3R in accordance with established nomenclature. We suggest that agl3R is one of a number of homologous proteins in Streptomyces (there are 57 putative GntR family regulators in the S. coelicolor genome) that respond to nutritional and/or environmental signals to control genes that affect morphogenesis and antibiotic production.
Hillerich
Brandan
B
Genetics Department, University of Georgia, Athens, 30602, USA.
Westpheling
Janet
J
D018528:ATP-Binding Cassette Transporters / Q000096:biosynthesis*; D000900:Anti-Bacterial Agents / Q000096:biosynthesis*; D019677:Artificial Gene Fusion; D050260:Carbohydrate Metabolism; D004269:DNA, Bacterial / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics; D024202:Electrophoretic Mobility Shift Assay; D029968:Escherichia coli Proteins / Q000032:analysis / Q000235:genetics; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D005809:Genes, Regulator; D017930:Genes, Reporter / Q000235:genetics; D005960:Glucosides / Q000378:metabolism; D009024:Morphogenesis; D011485:Protein Binding; D012329:RNA, Bacterial / Q000032:analysis / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D012097:Repressor Proteins / Q000235:genetics / Q000502:physiology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D048372:Streptomyces coelicolor / Q000235:genetics* / Q000254:growth & development; D027981:Symporters / Q000032:analysis; D014157:Transcription Factors / Q000235:genetics; D014158:Transcription, Genetic
D018528:ATP-Binding Cassette Transporters; D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins; D005960:Glucosides; C081598:GntR protein, E coli; D012329:RNA, Bacterial; D012333:RNA, Messenger; D012097:Repressor Proteins; D027981:Symporters; D014157:Transcription Factors; C033903:xylE protein, E coli