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Murat Elibol – One of the best experts on this subject based on the ideXlab platform.
optimization of medium composition for Actinorhodin production by streptomyces coelicolor a3 2 with response surface methodologyProcess Biochemistry, 2004Co-Authors: Murat ElibolAbstract:
Optimization of the fermentation medium for maximization of Actinorhodin production by Streptomyces coelicolor A3(2) was carried out. Response surface methodology (RSM) was applied to optimize the medium constituents. A 24 full-factorial central composite design (CCD) was chosen to explain the combined effects of the four medium constituents, viz. sucrose, glucose, yeast extract (YE) and peptone, and to design a minimum number of experiments. The P-values of the coefficients for linear, quadratic and cross-product effect of sucrose and glucose concentration were <0.0001, suggesting that these were critical variables having the greatest effect on the production of Actinorhodin in the complex medium. The optimized medium consisting of 339 g/l sucrose, 1 g/l glucose, 1.95 g/l YE and 2.72 g/l peptone predicted 195 mg/l of Actinorhodin which was 32% higher than that of the unoptimized medium. The amounts of glucose, YE and peptone required were also reduced with RSM.
response surface methodological approach for inclusion of perfluorocarbon in Actinorhodin fermentation mediumProcess Biochemistry, 2002Co-Authors: Murat ElibolAbstract:
The combined effects of perfluorocarbon and glucose concentrations on Actinorhodin production by Streptomyces coelicolor A3(2) were studied in a 2-l bioreactor using response surface methodology. A 22 full-factorial central composite design was employed for experimental design and analysis of the results. The optimum PFC and glucose concentrations were found to be 42.7% and 12.25 g/l, respectively. In these conditions, Actinorhodin concentration of 60 mg/l with a biomass concentration of 1.9 g/l, a maximum volumetric oxygen uptake rate of 180 mgO2/l h and a glucose consumption rate of 0.110 g glucose/l h was attained. These results are in close agreement with the model predictions.
A kinetic model for Actinorhodin production by Streptomyces coelicolor A3(2)Process Biochemistry, 1999Co-Authors: Murat Elibol, Ferda MavitunaAbstract:
Abstract The fermentation kinetics of an extracellular antibiotic, Actinorhodin, by Streptomyces coelicolor were studied in a batch system. A simple model was proposed using the Logistic equation for growth, the Luedeking–Piret equation for Actinorhodin production and Luedeking–Piret-like equations for glucose and oxygen consumptions. The model appeared to provide a reasonable description for each parameter during the growth phase.
Mervyn J. Bibb – One of the best experts on this subject based on the ideXlab platform.
Synthetic RNA silencing of Actinorhodin biosynthesis, 2016Co-Authors: Gabriel C. Uguru, Mervyn J. Bibb, Shan Goh, Liam Good, James E. M. StachAbstract:
We demonstrate the first application of synthetic RNA gene silencers in Streptomyces coelicolor A3(2). Peptide nucleic acid and expressed antisense RNA silencers successfully inhibited Actinorhodin production. Synthetic RNA silencing was target-specific and is a new tool for gene regulation and metabolic engineering studies in Streptomyces
Synthetic RNA Silencing of Actinorhodin Biosynthesis in Streptomyces coelicolor A3(2)PLoS ONE, 2013Co-Authors: Gabriel C. Uguru, Mervyn J. Bibb, Andrew Hesketh, Madhav Mondhe, Shan Goh, Liam Good, James E. M. StachAbstract:
We demonstrate the first application of synthetic RNA gene silencers in Streptomyces coelicolor A3(2). Peptide nucleic acid and expressed antisense RNA silencers successfully inhibited Actinorhodin production. Synthetic RNA silencing was target-specific and is a new tool for gene regulation and metabolic engineering studies in Streptomyces.
the role of absc a novel regulatory gene for secondary metabolism in zinc dependent antibiotic production in streptomyces coelicolor a3 2Molecular Microbiology, 2009Co-Authors: Andrew Hesketh, Holger Kock, Saraspadee Mootien, Mervyn J. BibbAbstract:
The availability of zinc was shown to have a marked influence on the biosynthesis of Actinorhodin in Streptomyces coelicolor A3(2). Production of Actinorhodin and undecylprodigiosin was abolished when a novel pleiotropic regulatory gene, absC, was deleted, but only when zinc concentrations were low. AbsC was shown to control expression of the gene cluster encoding production of coelibactin, an uncharacterized non-ribosomally synthesized peptide with predicted siderophore-like activity, and the observed defect in antibiotic production was found to result from elevated expression of this gene cluster. Promoter regions in the coelibactin cluster contain predicted binding motifs for the zinc-responsive regulator Zur, and dual regulation of coelibactin expression by zur and absC was demonstrated using strains engineered to contain deletions in either or both of these genes. An AbsC binding site was identified in a divergent promoter region within the coelibactin biosynthetic gene cluster, adjacent to a putative Zur binding site. Repression of the coelibactin gene cluster by both AbsC and Zur appears to be required to maintain appropriate intracellular levels of zinc in S. coelicolor.
Wendy Champness – One of the best experts on this subject based on the ideXlab platform.
global negative regulation of streptomyces coelicolor antibiotic synthesis mediated by an absa encoded putative signal transduction systemJournal of Bacteriology, 1996Co-Authors: Paul Brian, Perry Riggle, R A Santos, Wendy ChampnessAbstract:
Streptomycete antibiotic synthesis is coupled to morphological differentiation such that antibiotics are produced as a colony sporulates. Streptomyces coelicolor produces several structurally and genetically distinct antibiotics. The S. coelicolor absA locus was defined by four UV-induced mutations that globally blocked antibiotic biosynthesis without blocking morphological differentiation. We show that the absA locus encodes a putative eubacterial two-component sensor kinase-response regulator system. All four mutations lie within a single open reading frame, designated absA1, which is predicted to encode a sensor histidine kinase. A second gene downstream of absA1, absA2, is predicted to encode the cognate response regulator. In marked contrast to the antibiotic-deficient phenotype of the previously described absA mutants, the phenotype caused by disruption mutations in the absA locus is precocious hyperproduction of the antibiotics Actinorhodin and undecylprodigiosin. Precocious hyperproduction of these antibiotics is correlated with premature expression of XylE activity in a transcriptional fusion to an Actinorhodin biosynthetic gene. We propose that the absA locus encodes a signal transduction mechanism that negatively regulates synthesis of the multiple antibiotics produced by S. coelicolor.