Activation of the actinorhodin biosynthetic pathway in Streptomyces lividans

Romero, Nicolás

doi:10.1016/0378-1097(95)00041-3

Cited by 10 publications

(15 citation statements)

References 6 publications

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“…Also, a probable acyl-CoA dehydrogenase (SCO6938) belonging to this island has been implicated in control of actinorhodin production and timing of sporulation [38]. This observation is particularly interesting considering the extremely low-levels of actinorhodin production [39] and absence (or silencing) of the ram -independent developmental pathway in S. lividans [40]. Furthermore, two putative DNA methylases (SCO6844 and SCO6885) also map to this locus.…”

Section: Resultsmentioning

confidence: 99%

Comparative genomic hybridizations reveal absence of large Streptomyces coelicolor genomic islands in Streptomyces lividans

et al. 2007

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Background: The genomes of Streptomyces coelicolor and Streptomyces lividans bear a considerable degree of synteny. While S. coelicolor is the model streptomycete for studying antibiotic synthesis and differentiation, S. lividans is almost exclusively considered as the preferred host, among actinomycetes, for cloning and expression of exogenous DNA. We used whole genome microarrays as a comparative genomics tool for identifying the subtle differences between these two chromosomes.

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Section: Resultsmentioning

confidence: 99%

Comparative genomic hybridizations reveal absence of large Streptomyces coelicolor genomic islands in Streptomyces lividans

et al. 2007

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“…To date, several genes have been reported to activate the production of actinorhodin in S. coelicolor A3(2) or its close relative S. lividans. Thus, introduction by a multicopy plasmid of the gene afsR (25) or abaA (14) or an activator gene from S. lividans (47) activates actinorhodin production in S. lividans, while mutational disruption of the absA locus results in precocious hyperproduction of actinorhodin and undecylprodigiosin in S. coelicolor A3(2) (3). The presumed functions of afsR, abaA, and absA, however, do not involve the ribosome.…”

Section: Discussionmentioning

confidence: 99%

“…The presumed functions of afsR, abaA, and absA, however, do not involve the ribosome. The activator gene from S. lividans is reported to encode an 86-nucleotide transcript, and this may act as an antisense RNA, blocking synthesis of a putative repressor protein (47). A tetracycline-resistant mutant of Streptomyces granaticolor has been reported to overproduce (twofold) granaticins (52).…”

Section: Discussionmentioning

confidence: 99%

Induction of actinorhodin production by rpsL (encoding ribosomal protein S12) mutations that confer streptomycin resistance in Streptomyces lividans and Streptomyces coelicolor A3(2)

et al. 1996

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A strain of Streptomyces lividans, TK24, was found to produce a pigmented antibiotic, actinorhodin, although S. lividans normally does not produce this antibiotic. Genetic analyses revealed that a streptomycin-resistant mutation str-6 in strain TK24 is responsible for induction of antibiotic synthesis. DNA sequencing showed that str-6 is a point mutation in the rpsL gene encoding ribosomal protein S12, changing Lys-88 to Glu. Gene replacement experiments with the Lys883Glu str allele demonstrated unambiguously that the str mutation is alone responsible for the activation of actinorhodin production observed. In contrast, the strA1 mutation, a genetic marker frequently used for crosses, did not restore actinorhodin production and was found to result in an amino acid alteration of Lys-43 to Asn. Induction of actinorhodin production was also detected in strain TK21, which does not harbor the str-6 mutation, when cells were incubated with sufficient streptomycin or tetracycline to reduce the cell's growth rate, and 40 and 3% of streptomycin-or tetracycline-resistant mutants, respectively, derived from strain TK21 produced actinorhodin. Streptomycin-resistant mutations also blocked the inhibitory effects of relA and brgA mutations on antibiotic production, aerial mycelium formation or both. These str mutations changed Lys-88 to Glu or Arg and Arg-86 to His in ribosomal protein S12. The decrease in streptomycin production in relC mutants in Streptomyces griseus could also be abolished completely by introducing streptomycin-resistant mutations, although the impairment in antibiotic production due to bldA (in Streptomyces coelicolor) or afs mutations (in S. griseus) was not eliminated. These results indicate that the onset and extent of secondary metabolism in Streptomyces spp. is significantly controlled by the translational machinery.

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“…In Streptomyces lividans, a species closely related to S. coelicolor, all of the genetic components for actinorhodin biosynthesis have also been identified, but actinorhodin is not produced under usual growth conditions (32). Because of this trait, the focus of study in this strain has been on how actinorhodin biosynthesis is initiated and regulated.…”

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confidence: 99%

Accumulation ofS-Adenosyl-l-Methionine Enhances Production of Actinorhodin but Inhibits Sporulation inStreptomyces lividansTK23

et al. 2003

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S-Adenosyl-L-methionine synthetase (SAM-s) catalyzes the biosynthesis of SAM from ATP and L-methionine. Despite extensive research with many organisms, its role in Streptomyces sp. remains unclear. In the present study, the putative SAM-s gene was isolated from a spectinomycin producer, Streptomyces spectabilis. The purified protein from the transformed Escherichia coli with the isolated gene synthesized SAM from L-methionine and ATP in vitro, strongly indicating that the isolated gene indeed encoded the SAM-s protein.The overexpression of the SAM-s gene in Streptomyces lividans TK23 inhibited sporulation and aerial mycelium formation but enhanced the production of actinorhodin in both agar plates and liquid media. Surprisingly, the overexpressed SAM was proven by Northern analysis to increase the production of actinorhodin through the induction of actII-ORF4, a transcription activator of actinorhodin biosynthetic gene clusters. In addition, we found that a certain level of intracellular SAM is critical for the induction of antibiotic biosynthetic genes, since the control strain harboring only the plasmid DNA did not show any induction of actII-ORF4 until it reached a certain level of SAM in the cell. From these results, we concluded that the SAM plays important roles as an intracellular factor in both cellular differentiation and antibiotic production in Streptomyces sp.

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Activation of the actinorhodin biosynthetic pathway in Streptomyces lividans

Cited by 10 publications

References 6 publications

Comparative genomic hybridizations reveal absence of large Streptomyces coelicolor genomic islands in Streptomyces lividans

Comparative genomic hybridizations reveal absence of large Streptomyces coelicolor genomic islands in Streptomyces lividans

Induction of actinorhodin production by rpsL (encoding ribosomal protein S12) mutations that confer streptomycin resistance in Streptomyces lividans and Streptomyces coelicolor A3(2)

Accumulation ofS-Adenosyl-l-Methionine Enhances Production of Actinorhodin but Inhibits Sporulation inStreptomyces lividansTK23

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