Induction of the Bacillus subtilis SOS-like response by Escherichia coli RecA protein.

Love, Paul E.; Yasbin, Ronald E.

doi:10.1073/pnas.83.14.5204

Cited by 45 publications

(51 citation statements)

References 39 publications

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“…Overexpression of E. coli RecA protein can complement the deficiency in din gene induction in strains of B. subtilis carrying the recA4 mutation (5,22). In addition, RecA of B. subtilis can facilitate the inactivation of LexA repressor in vitro (25).…”

Section: Resultsmentioning

confidence: 99%

Cloning and characterization of DNA damage-inducible promoter regions from Bacillus subtilis

1991

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DNA damage-inducible (din) (16,41). Regulation of the SOS system in E. coli is controlled by the products of the recA and lexA genes. The RecA protein has many functions in E. coli and is involved in the processes of recombination, DNA repair, and mutagenesis (31,41,45). The LexA protein is a repressor of as many as 20 unlinked, coordinately regulated loci which include the recA and lexA genes themselves (19,41). Following exposure of E. coli to agents that alter DNA structure or interfere with DNA replication (such as UV radiation, mitomycin, nalidixic acid, etc.), an inducing signal is generated. (4,7,17,34,35), and the UmuD protein (2, 39). As levels of LexA repressor decline, damage-inducible loci are derepressed, resulting in expression of'the physiological phenomena that compose the SOS response (16, 41).The SOS system of E. coli has served as a model for the study of similar inducible DNA repair systems in other gram-negative bacteria (14,36,37,43,44 and essentially error free (7a). This contrasts with W reactivation in E. coli, which is capable of repairing a variety of DNA lesions by an error-prone mechanism (32). Furthermore, while induction of all SOS phenomena in E. coli is dependent upon a functional RecA protein, filamentation in B. subtilis is a RecA-independent response (21). Finally, the SOB system in B. subtilis is developmentally regulated. As B. subtilis differentiates into the physiological state of natural competence (6), SOB phenomena are spontaneously induced in the absence of externally generated DNA damage (20,23,47,49,50).DNA damage-inducible loci in B. subtilis were first identified by using transposon-mediated gene fusions (20). Tn917-lacZ transposon insertions within din loci were isolated from a library of insertions by selecting those fusions that induced expression of the lacZ reporter gene after exposure to DNA-damaging agents (20). Fifteen independently isolated din gene transposon insertions were genetically mapped and localized to three loci (dinA, dinB, and dinC) on the B. subtilis chromosome (11). As mentioned above, induction of all three din loci was demonstrated to be dependent upon a functional RecA protein (20). In order to elucidate the mechanisms that regulate damage-inducible gene expression in B. subtilis, we have cloned and sequenced DNA fragments that contain the dinA, dinB, and dinC promoter regions. Described here is our initial characterization of these cloned din promoter regions and the identification of a putative SOB operator sequence.

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Section: Resultsmentioning

confidence: 99%

Cloning and characterization of DNA damage-inducible promoter regions from Bacillus subtilis

1991

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“…An open reading frame (ORF) whose translation had homology to E. coli RecA and which spanned the Sstl site thought to be internal to the gene by DNA (2) and the posttranslational conversion of UmuD to UmuD' (8,44,53). A further role of RecA protein in UV-induced mutagenesis has also been identified (44) (35), whereas the reverse is true of E. coli RecA, which does not stimulate the induction of bacillus prophages (34).…”

Section: Resultsmentioning

confidence: 99%

Novel structure of the recA locus of Mycobacterium tuberculosis implies processing of the gene product

1991

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A fragment of Mycobacterium tuberculosis DNA containing recA-like sequences was identified by hybridization with the Escherichia coli recA gene and cloned. Although no expression was detected from its own promoter in E. coli, expression from a vector promoter partially complemented E. coli recA mutants for recombination, DNA repair, and mutagenesis, but not for induction of phage K. This clone produced a protein which cross-reacts with antisera raised against the E. coli RecA protein and was approximately the same size. However, the nucleotide sequence of the cloned fragment revealed the presence of an open reading frame for a protein about twice the size of other RecA proteins and the cloned product detected by Western blotting (immunoblotting). The predicted M. tuberculosis RecA protein sequence was homologous with RecA sequences from other bacteria, but this homology was not dispersed; rather it was localized to the first 254 and the last 96 amino acids, with the intervening 440 amino acids being unrelated. Furthermore, the junctions of homology were in register with the uninterrupted sequence Qf the E. coli RecA protein. Identical restriction fragments were found in the genomic DNAs of M. tuberculosis H37Rv and H37Ra and of M. bovis BCG. It is concluded that the ancestral recA gene of these species diversified via an insertional mutation of at least 1,320 bp of DNA. Possible processing mechanisms for synthesizing a normal-size RecA protein from this elongated sequence are discussed.

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“…Competent bacteria exhibit new properties with regard to surface antigens (Nava et al, 1963), membrane nuclease activity (Lacks & Greenberg, 1973;Lacks & Neuberger, 1975), DNA transport (Lerman 8z Tolmach, 1957), recombination and repair (Love & Yasbin, 1986), expression of a set of specific proteins (Morrison & Baker, 1979;Raina & Ravin, 1980) and synthesis of the lipid polymer poly(P-hydroxybutyrate) (Reusch & Sadoff, 1983 ; ClavC et al, 1989). Membrane hyperpolarization (Trombe, 1983), as well as a stimulation of glycolysis associated with an increased ATP pool and a cytoplasmic alkalinization (Lopez et al, 1989), are observed in competent S .…”

Section: Introductionmentioning

confidence: 99%

Calcium regulation of growth and differentiation in Streptococcus pneumoniae

Trombe

Clavé²,

Manias³

1992

Journal of General Microbiology

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Streptococcus pneumonk requires 0.15 mM-Ca2+ in the medium for optimal growth. Increasing the Ca2+ concentration to 1 mM triggers either a differentiathe state, competence for genetic transformation during exponential growth, or partial lysis as won as the cultures enter stationary phase. Genetic and physiological data both suggest that these responses are under the control of activator@), excreted in the presence of high Ca2+ concentrations. 45Ca2+ transport is also stimulated by the activator(s). The amiloride derivative 2',4-dimethylbenzarnil (DMB) inhibits 45Ca2+ transport and prevents lysis and competence development. This provides evidence in favour of the involvement of Ca2+ transport in competence and culture lysis. On the other hand, addition of DNA to a competent culture prevents lysis of wild-type bacteria while a mutant, defective for DNA uptake, is not protected from lysis by exogenous DNA. An hypothesis is proposed for competence induction as a global metabolic response to Ca2+, under the control of competence factor.

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Induction of the Bacillus subtilis SOS-like response by Escherichia coli RecA protein.

Cited by 45 publications

References 39 publications

Cloning and characterization of DNA damage-inducible promoter regions from Bacillus subtilis

Cloning and characterization of DNA damage-inducible promoter regions from Bacillus subtilis

Novel structure of the recA locus of Mycobacterium tuberculosis implies processing of the gene product

Calcium regulation of growth and differentiation in Streptococcus pneumoniae

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