Angela Forero, Mauricio Sánchez, Adán Chávez, Beatriz Ruiz, Romina Rodríguez-Sanoja, Luis Servín-González, Sergio Sánchez
Departamento de Biología Molecular y Biotecnología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, D.F. 04510, México.
Canadian journal of microbiology 2012 OctStreptomyces coelicolor mutants resistant to 2-deoxyglucose are insensitive to carbon catabolite repression (CCR). Total reversion to CCR sensitivity is observed by mutant complementation with a DNA region harboring both glucose kinase glkA gene and the sco2127 gene. The sco2127 is located upstream of glkA and encodes a putative protein of 20.1 kDa. In S. coelicolor, actinorhodin production is subject to glucose repression. To explore the possible involvement of both SCO2127 and glucose kinase (Glk) in the glucose sensitivity of actinorhodin production, this effect was evaluated in a wild-type S. coelicolor A3(2) M145 strain and a sco2127 null mutant (Δsco2127) derived from this wild-type strain. In comparison with strain M145, actinorhodin production by the mutant was insensitive to glucose repression. Under repressive conditions, only minor differences were observed in glucose utilization and Glk production between these strains. SCO2127 was detected mainly during the first 36 h of fermentation, just before the onset of antibiotic production, and its synthesis was not related to a particular carbon source. The glucose sensitivity of antibiotic production was restored to wild-type phenotype by transformation with an integrative plasmid containing sco2127. Our results support the hypothesis that SCO2127 is a negative regulator of actinorhodin production and suggest that the effect is independent of Glk.
Angela Forero, Mauricio Sánchez, Adán Chávez, Beatriz Ruiz, Romina Rodríguez-Sanoja, Luis Servín-González, Sergio Sánchez. Possible involvement of the sco2127 gene product in glucose repression of actinorhodin production in Streptomyces coelicolor. Canadian journal of microbiology. 2012 Oct;58(10):1195-201
PMID: 23051184
View Full Text