The glucose kinase gene of Streptomyces coelicolor A3(2): its nucleotide sequence, transcriptional analysis and role in glucose repression

1992 ◽  
Vol 6 (19) ◽  
pp. 2833-2844 ◽  
Author(s):  
S. Angell ◽  
E. Schwarz ◽  
M. J. Bibb
Keyword(s):  
Nucleotide Sequence ◽  
Glucose Repression ◽  
Streptomyces Coelicolor ◽  
Transcriptional Analysis ◽  
Kinase Gene ◽  
Glucose Kinase

scholarly journals glkA Is Involved in Glucose Repression of Chitinase Production in Streptomyces lividans

1998 ◽  
Vol 180 (11) ◽  
pp. 2911-2914 ◽  
Author(s):  
Akihiro Saito ◽  
Takeshi Fujii ◽  
Tadakatsu Yoneyama ◽  
Kiyotaka Miyashita
Keyword(s):  
Sole Carbon Source ◽  
Glucose Repression ◽  
Streptomyces Coelicolor ◽  
Streptomyces Lividans ◽  
Transcriptional Analysis ◽  
Copy Number Plasmid ◽  
Low Copy Number ◽  
Chitinase Production ◽  
Dna Fragment ◽  
Glucose Kinase

ABSTRACT Chitinase production in Streptomyces lividans is induced by chitin and repressed in the presence of glucose. A mutant ofS. lividans TK24, strain G015, which was defective in glucose repression of chitinase production, was obtained by screening colonies for zones of clearing on colloidal chitin agar plates containing 1.0% (wt/vol) glucose. The transcriptional analysis ofchiA in G015 with xylE, which encodes catechol 2,3-dioxygenase, as a reporter gene showed that the transcription from the chiA promoter of S. lividans TK24 occurred regardless of the presence of glucose. G015 was resistant to 2-deoxyglucose (2-DOG) and did not utilize glucose as a sole carbon source. When a DNA fragment containing glkA, a gene for glucose kinase, of Streptomyces coelicolor A3(2) was introduced into strain G015 on a low-copy-number plasmid, the sensitivity to 2-DOG, the ability to utilize glucose, and the glucose repression of chitinase production were restored. These results indicate that glkA is involved in glucose repression of chitinase production in S. lividans TK24.

Glucose repression in Streptomyces coelicolor A3(2): a likely regulatory role for glucose kinase

1994 ◽  
Vol 244 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Susan Angell ◽  
Cinzia G. Lewis ◽  
Mark J. Buttner ◽  
Mervyn J. Bibb
Keyword(s):  
Glucose Repression ◽  
Streptomyces Coelicolor ◽  
Regulatory Role ◽  
Glucose Kinase

Possible involvement of the sco2127 gene product in glucose repression of actinorhodin production in Streptomyces coelicolor

2012 ◽  
Vol 58 (10) ◽  
pp. 1195-1201 ◽  
Author(s):  
Angela Forero ◽  
Mauricio Sánchez ◽  
Adán Chávez ◽  
Beatriz Ruiz ◽  
Romina Rodríguez-Sanoja ◽  
...  
Keyword(s):  
Glucose Repression ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Negative Regulator ◽  
Wild Type ◽  
Wild Type Phenotype ◽  
Glucose Sensitivity ◽  
Mutant Complementation ◽  
Glucose Kinase ◽  
Actinorhodin Production

Streptomyces 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.

scholarly journals In Vivo Analysis of HPr Reveals a Fructose-Specific Phosphotransferase System That Confers High-Affinity Uptake in Streptomyces coelicolor

2003 ◽  
Vol 185 (3) ◽  
pp. 929-937 ◽  
Author(s):  
Harald Nothaft ◽  
Stephan Parche ◽  
Annette Kamionka ◽  
Fritz Titgemeyer
Keyword(s):  
Carbon Source ◽  
Glucose Repression ◽  
Streptomyces Coelicolor ◽  
Carbon Sources ◽  
Glycerol Kinase ◽  
Transcriptional Analysis ◽  
Phosphotransferase System ◽  
Gram Positive ◽  
High Affinity

ABSTRACT HPr, the histidine-containing phosphocarrier protein of the bacterial phosphotransferase system (PTS), serves multiple functions in carbohydrate uptake and carbon source regulation in low-G+C-content gram-positive bacteria and in gram-negative bacteria. To assess the role of HPr in the high-G+C-content gram-positive organism Streptomyces coelicolor, the encoding gene, ptsH, was deleted. The ptsH mutant BAP1 was impaired in fructose utilization, while growth on other carbon sources was not affected. Uptake assays revealed that BAP1 could not transport appreciable amounts of fructose, while the wild type showed inducible high-affinity fructose transport with an apparent Km of 2 μM. Complementation and reconstitution experiments demonstrated that HPr is indispensable for a fructose-specific PTS activity. Investigation of the putative fruKA gene locus led to identification of the fructose-specific enzyme II permease encoded by the fruA gene. Synthesis of HPr was not specifically enhanced in fructose-grown cells and occurred also in the presence of non-PTS carbon sources. Transcriptional analysis of ptsH revealed two promoters that are carbon source regulated. In contrast to what happens in other bacteria, glucose repression of glycerol kinase was still operative in a ptsH background, which suggests that HPr is not involved in general carbon regulation. However, fructose repression of glycerol kinase was lost in BAP1, indicating that the fructose-PTS is required for transduction of the signal. This study provides the first molecular genetic evidence of a physiological role of the PTS in S. coelicolor.

Genetic mapping, cloning and physiological aspects of the glucose kinase gene of Streptomyces coelicolor

1984 ◽  
Vol 196 (3) ◽  
pp. 501-507 ◽  
Author(s):  
Haruo Ikeda ◽  
Eugene T. Seno ◽  
Celia J. Bruton ◽  
Keith F. Chater
Keyword(s):  
Genetic Mapping ◽  
Streptomyces Coelicolor ◽  
Kinase Gene ◽  
Glucose Kinase
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