recA gene of Escherichia coli complements defects in DNA repair and mutagenesis in Streptomyces fradiae JS6 (mcr-6)

Matsushima, Patti; Baltz, Richard H.

doi:10.1128/jb.169.10.4834-4836.1987

Cited by 15 publications

(5 citation statements)

References 30 publications

(36 reference statements)

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“…Early attempts to isolate tee-mutants of Streptomyces coelicolor A3(2) led to the identification of six geneloci, but none of the mutations had a clear-cut effect on recombination capability in crosses [3,4]. In Streptomyces fradiae a mutant (JS6) was isolated that was defective in repair of DNA damage and error-prone DNA repair and could be complemented with the recA gene of E. coli [5]. However, no effect of the mutation on recombination in S. fradiae has been reported.…”

Section: Introductionmentioning

confidence: 99%

Identification, isolation and sequencing of the recA gene of Streptomyces lividans TK24

Nuβbaumer¹

1994

FEMS Microbiology Letters

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An internal fragment of the recA gene of Streptomyces cattleya was amplified by the polymerase chain reaction (PCR) employing degenerate oligonucleotide primers. Using this fragment as a hybridization probe, a recA homologous gene could be shown in each tested Streptomyces strain. A 4.4 kb BamHI fragment which carried the complete recA gene was isolated from Streptomyces lividans TK24. Sequence analysis suggested that the coding region of the recA gene consists of 1122 bp. The highest similarity (approximately 78%) could be detected to the recA genes of Mycobacterium tuberculosis and Mycobacterium leprae. After fusion with an E. coli promoter the S. lividans recA gene could partially complement an Escherichia coli recA mutant.

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Section: Introductionmentioning

confidence: 99%

Identification, isolation and sequencing of the recA gene of Streptomyces lividans TK24

Nuβbaumer¹

1994

FEMS Microbiology Letters

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“…Furthermore, S. fradiae has a recA gene functionally complementable by E. coli recA. 8 These studies were facilitated by the use of antibioticresistance markers, including resistance to Rifampicin (RifR), spectinomycin (SpcR) and streptomycin (StrR), to monitor the frequencies of mutation in different strains and with different mutagenic agents.…”

Section: Introductionmentioning

confidence: 99%

Spontaneous and induced mutations to rifampicin, streptomycin and spectinomycin resistances in actinomycetes: mutagenic mechanisms and applications for strain improvement

Baltz¹

2014

J Antibiot

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Chemical mutagenesis continues to be an important foundational methodology for the generation of highly productive actinomycete strains for the commercial production of antibiotics and other secondary metabolites. In the past, the determination of frequencies of chemically induced resistance to rifampicin (RifR), spectinomycin (SpcR) and streptomycin (StrR) have served as surrogate markers to monitor the efficiencies and robustness of mutagenic protocols. Recent studies indicate that high level RifR, SpcR and StrR phenotypes map to specific regions of the rpoB, rpsE and rpsL genes, respectively, in actinomycetes. Moreover, mutagenesis to RifR can occur spontaneously at many different sites in rpoB, and all six types of base-pair substitutions, as well as in-frame deletions and insertions, have been observed. The RifR/rpoB system provides a robust method to rank mutagenic protocols, to evaluate mutagen specificity and to study spontaneous mutagenesis mechanisms involved in the maintenance of high G+C content in Streptomyces species and other actinomycetes.

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“…Stonesifer and Baltz (1985) isolated an S. fradiae mutant, JS6, that was impaired in DNA repair and UV-induced mutagenesis. This mutant could be complemented by the E. coli recA gene (Matsushima and Baltz 1987), but its ability to undergo homologous recombination was not tested. The S. lividans mutant JT46 (Tsai and Chen 1987) tolerates plasmids with repetitive sequences but is impaired only in intraplasmid recombination, not in general homologous recombination (Kieser et al 1989).…”

Section: Introductionmentioning

confidence: 99%

Mutational analysis of the Streptomyces lividans recA gene suggests that only mutants with residual activity remain viable

et al. 1997

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Temperature-sensitive integration plasmids carrying internal fragments of the Streptomyces lividans TK24 recA gene were constructed and used to inactivate the chromosomal recA gene of S. lividans by gene disruption and gene replacement. Integration of these plasmids resulted in recA mutants expressing C-terminally truncated RecA proteins, as deduced from Southern hybridization experiments. Mutants FRECD2 in which the last 42 amino acids, comprising the variable part of bacterial RecA proteins, had been deleted retained the wild-type phenotype. The S. lividans recA mutant FRECD3 produced a RecA protein lacking 87 amino acids probably including the interfilament contact site. FRECD3 was more sensitive to UV and MMS than the wild-type. Its ability to undergo homologous recombination was impaired, but not completely abolished. Integration of the disruption plasmid pFRECD3 in S. coelicolor "Müller" caused the same mutant phenotype as S. lividans FRECD3. In spite of many attempts no S. lividans recA mutants with deletions of 165 C-terminal amino acids or more were isolated. Furthermore, the recA gene could not be replaced by a kanamycin resistance cassette. These experiments indicate a crucial role of the recA gene in ensuring viability of Streptomyces.

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recA gene of Escherichia coli complements defects in DNA repair and mutagenesis in Streptomyces fradiae JS6 (mcr-6)

Cited by 15 publications

References 30 publications

Identification, isolation and sequencing of the recA gene of Streptomyces lividans TK24

Identification, isolation and sequencing of the recA gene of Streptomyces lividans TK24

Spontaneous and induced mutations to rifampicin, streptomycin and spectinomycin resistances in actinomycetes: mutagenic mechanisms and applications for strain improvement

Mutational analysis of the Streptomyces lividans recA gene suggests that only mutants with residual activity remain viable

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