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 EshA Accentuates ppGpp Accumulation and Is Conditionally Required for Antibiotic Production in Streptomyces coelicolor A3(2)

2006 ◽  
Vol 188 (13) ◽  
pp. 4952-4961 ◽  
Author(s):  
Natsumi Saito ◽  
Jun Xu ◽  
Takeshi Hosaka ◽  
Susumu Okamoto ◽  
Hiroyuki Aoki ◽  
...  
Keyword(s):  
Type Strain ◽  
Wild Type Strain ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Molecular Signaling ◽  
Wild Type ◽  
Nucleotide Binding Domain ◽  
In The Wild ◽  
Actinorhodin Production ◽  
Cyclic Nucleotide Binding Domain

ABSTRACT Disruption of eshA, which encodes a 52-kDa protein that is produced late during the growth of Streptomyces coelicolor A3(2), resulted in elimination of actinorhodin production. In contrast, disruption of eshB, a close homologue of eshA, had no effect on antibiotic production. The eshA disruptant accumulated lower levels of ppGpp than the wild-type strain accumulated. The loss of actinorhodin production in the eshA disruptant was restored by expression of a truncated relA gene, which increased the ppGpp level to the level in the wild-type strain, indicating that the reduced ppGpp accumulation in the eshA mutant was solely responsible for the loss of antibiotic production. Antibiotic production was also restored in the eshA mutant by introducing mutations into rpoB (encoding the RNA polymerase β subunit) that bypassed the requirement for ppGpp, which is consistent with a role for EshA in modulating ppGpp levels. EshA contains a cyclic nucleotide-binding domain that is essential for its role in triggering actinorhodin production. EshA may provide new insights and opportunities to unravel the molecular signaling events that occur during physiological differentiation in streptomycetes.

scholarly journals Role of Phosphopantetheinyl Transferase Genes in Antibiotic Production by Streptomyces coelicolor

2008 ◽  
Vol 190 (20) ◽  
pp. 6903-6908 ◽  
Author(s):  
Ya-Wen Lu ◽  
Adrianna K. San Roman ◽  
Amy M. Gehring
Keyword(s):  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Morphological Development ◽  
Phosphopantetheinyl Transferase ◽  
Calcium Dependent ◽  
Actinorhodin Production

ABSTRACT The phosphopantetheinyl transferase genes SCO5883 (redU) and SCO6673 were disrupted in Streptomyces coelicolor. The redU mutants did not synthesize undecylprodigiosin, while SCO6673 mutants failed to produce calcium-dependent antibiotic. Neither gene was essential for actinorhodin production or morphological development in S. coelicolor, although their mutation could influence these processes.

scholarly journals New Sporulation Loci in Streptomyces coelicolor A3(2)

1999 ◽  
Vol 181 (17) ◽  
pp. 5419-5425 ◽  
Author(s):  
N. Jamie Ryding ◽  
Maureen J. Bibb ◽  
Virginie Molle ◽  
Kim C. Findlay ◽  
Keith F. Chater ◽  
...  
Keyword(s):  
Phase Contrast ◽  
Streptomyces Coelicolor ◽  
Cosmid Library ◽  
Phase Contrast Microscopy ◽  
Wild Type ◽  
Chromosomal Dna ◽  
East Anglia ◽  
Wild Type Phenotype ◽  
Contrast Microscopy ◽  
Spore Pigment

ABSTRACT Sporulation mutants of Streptomyces coelicolor appear white because they are defective in the synthesis of the grey polyketide spore pigment, and such white (whi) mutants had been used to define eight sporulation loci, whiA,whiB, whiD, whiE, whiG,whiH, whiI, and whiJ (K. F. Chater, J. Gen. Microbiol. 72:9–28, 1972; N. J. Ryding, Ph.D. thesis, University of East Anglia, 1995). In an attempt to identify new whi loci, we mutagenized S. coelicolor M145 spores with nitrosoguanidine and identified 770 mutants with colonies ranging from white to medium grey. After excluding unstable strains, we examined the isolates by phase-contrast microscopy and chose 115 whi mutants with clear morphological phenotypes for further study. To exclude mutants representing cloned whi genes, self-transmissible SCP2*-derived plasmids carrying whiA, whiB,whiG, whiH, or whiJ (but notwhiD, whiE, or whiI) were introduced into each mutant by conjugation, and strains in which the wild-type phenotype was restored either partially or completely by any of these plasmids were excluded from further analysis. In an attempt to complement some of the remaining 31 whi mutants, an SCP2* library of wild-type S. coelicolor chromosomal DNA was introduced into 19 of the mutants by conjugation. Clones restoring the wild-type phenotype to 12 of the 19 strains were isolated and found to represent five distinct loci, designated whiK,whiL, whiM, whiN, andwhiO. Each of the five loci was located on the ordered cosmid library: whiL, whiM, whiN, and whiO occupied positions distinct from previously clonedwhi genes; whiK was located on the same cosmid overlap as whiD, but the two loci were shown by complementation to be distinct. The phenotypes resulting from mutations at each of these new loci are described.

scholarly journals RNase III Is Required for Actinomycin Production in Streptomyces antibioticus

2013 ◽  
Vol 79 (20) ◽  
pp. 6447-6451 ◽  
Author(s):  
Jung-Hoon Lee ◽  
Marcha L. Gatewood ◽  
George H. Jones
Keyword(s):  
Parental Strain ◽  
Insertional Mutagenesis ◽  
Southern Blotting ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Production Medium ◽  
Wild Type ◽  
Rnase Iii ◽  
Content Type ◽  
Streptomyces Antibioticus

ABSTRACTUsing insertional mutagenesis, we have disrupted the RNase III gene,rnc, of the actinomycin-producing streptomycete,Streptomyces antibioticus. Disruption was verified by Southern blotting. The resulting strain grows more vigorously than its parent on actinomycin production medium but produces significantly lower levels of actinomycin. Complementation of therncdisruption with the wild-typerncgene fromS. antibioticusrestored actinomycin production to nearly wild-type levels. Western blotting experiments demonstrated that the disruptant did not produce full-length or truncated forms of RNase III. Thus, as is the case inStreptomyces coelicolor, RNase III is required for antibiotic production inS. antibioticus. No differences in the chemical half-lives of bulk mRNA were observed in a comparison of theS. antibioticus rncmutant and its parental strain.

An aberrant protein synthesis activity is linked with antibiotic overproduction in rpsL mutants of Streptomyces coelicolor A3(2)

Microbiology ◽  
2003 ◽  
Vol 149 (11) ◽  
pp. 3299-3309 ◽  
Author(s):  
Yoshiko Okamoto-Hosoya ◽  
Takeshi Hosaka ◽  
Kozo Ochi
Keyword(s):  
Protein Synthesis ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Translation System ◽  
In The Wild ◽  
Synthesis Activity ◽  
Aberrant Protein ◽  
Ribosomal Protein S12 ◽  
High Level ◽  
Actinorhodin Production

Certain mutations in the rpsL gene (encoding the ribosomal protein S12) activate or enhance antibiotic production in various bacteria. K88E and P91S rpsL mutants of Streptomyces coelicolor A3(2), with an enhanced actinorhodin production, were found to exhibit an aberrant protein synthesis activity. While a high level of this activity (as determined by the incorporation of labelled leucine) was detected at the late stationary phase in the mutants, it decreased with age of the cells in the wild-type strain. In addition, the aberrant protein synthesis was particularly pronounced when cells were subjected to amino acid shift-down, and was independent of their ability to accumulate ppGpp. Ribosomes of K88E and P91S mutants displayed an increased accuracy in protein synthesis as demonstrated by the poly(U)-directed cell-free translation system, but so did K43N, K43T, K43R and K88R mutants, which were streptomycin resistant but showed no effect on actinorhodin production. This eliminates the possibility that the increased accuracy level is a cause of the antibiotic overproduction in the K88E and P91S mutants. The K88E and P91S mutant ribosomes exhibited an increased stability of the 70S complex under low concentrations of magnesium. The authors propose that the aberrant activation of protein synthesis caused by the increased stability of the ribosome is responsible for the remarkable enhancement of antibiotic production in the K88E and P91S mutants.

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

scholarly journals Identification of glucose kinase‐dependent and ‐independent pathways for carbon control of primary metabolism, development and antibiotic production in Streptomyces coelicolor by quantitative proteomics

2017 ◽  
Vol 105 (1) ◽  
pp. 175-175 ◽  
Author(s):  
Jacob Gubbens ◽  
Marleen M. Janus ◽  
Bogdan I. Florea ◽  
Herman S. Overkleeft ◽  
Gilles P. van Wezel
Keyword(s):  
Quantitative Proteomics ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Primary Metabolism ◽  
Carbon Control ◽  
Glucose Kinase

scholarly journals Transcriptome Analysis of an Antibiotic Downregulator Mutant and Synergistic Actinorhodin Stimulation via Disruption of a Precursor Flux Regulator inStreptomyces coelicolor

2011 ◽  
Vol 77 (5) ◽  
pp. 1872-1877 ◽  
Author(s):  
Seon-Hye Kim ◽  
Han-Na Lee ◽  
Hye-Jin Kim ◽  
Eung-Soo Kim
Keyword(s):  
Microarray Analysis ◽  
Transcriptome Analysis ◽  
Carbon Flux ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Actinorhodin Production

ABSTRACTThrough microarray analysis of an antibiotic-downregulator-deletedStreptomyces coelicolorΔwblAΔSCO1712 mutant, 28wblA- and SCO1712-dependent genes were identified and characterized. Among 14wblA- and SCO1712-independent genes, a carbon flux regulating 6-phosphofructokinase SCO5426 was additionally disrupted in the ΔwblAΔSCO1712 mutant and further stimulated actinorhodin production inS. coelicolor, implying that both regulatory and precursor flux pathways could be synergistically optimized for antibiotic production.

Deletion of TerD-domain-encoding genes: effect on Streptomyces coelicolor development

2012 ◽  
Vol 58 (10) ◽  
pp. 1221-1229 ◽  
Author(s):  
Édith Sanssouci ◽  
Sylvain Lerat ◽  
François Daigle ◽  
Gilles Grondin ◽  
François Shareck ◽  
...  
Keyword(s):  
Liquid Medium ◽  
Potential Role ◽  
Solid Medium ◽  
Antibiotic Production ◽  
Streptomyces Coelicolor ◽  
Developmental Patterns ◽  
Small Colony ◽  
Encoding Genes ◽  
Actinorhodin Production

TerD-domain-encoding genes (tdd genes) are highly represented in the Streptomyces coelicolor genome. One of these, the tdd8 gene, was recently shown to have a crucial influence on growth, differentiation, and spore development of this filamentous bacterium. The investigation of the potential role of tdd genes has been extended here to tdd7 (SCO2367) and tdd13 (SCO4277). Both genes are highly expressed in bacteria grown in liquid-rich medium (tryptic soy broth). However, the deletion of these genes in S. coelicolor showed contrasting effects regarding developmental patterns, sporulation, and antibiotic production. Deletion of the tdd7 gene induced a reduction of growth in liquid medium, wrinkling of the mycelium on solid medium, and poor spore and actinorhodin production. On the other hand, deletion of the tdd13 gene did not significantly affect growth in liquid medium but induced a small colony phenotype on solid medium with abundant sporulation and overproduction of undecylprodigiosin. Although their exact functions remain undefined, the present data suggest a major involvement of TerD proteins in the proper development of S. coelicolor.

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