Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three DNA-dependent ATPases (gamma phosphohydrolases) can be isolated from Bacillus subtilis cells. We studied these enzymes in a number of mutants deficient in recombination or repair functions (rec, uvr) and in competent cells. The recA mutant studied had lower ATPase II activity, while competent cells had higher ATPase I activity, in comparison with the parental strain not brought to competence.
J Gen Microbiol 1984 Jan
PMID:DNA-dependent ATPases in Bacillus subtilis mutants and in competent cells. 614 20

Escherichia coli cells in which the recA promoter is fused to a lac structural gene, (Mu) Mud(Ap,lac)::rec, were irradiated with two far-ultraviolet light wavelengths (254 and 290 nm), selected monochromatic near-ultraviolet (NUV) wavelengths 313 nm, 334 nm, 365 nm, or broad band solar-UV (290-420 nm) from a solar simulator. Irradiation with the two far-ultraviolet wavelengths was followed by high yields of beta-galactosidase, lambda prophage induction, and Weigle reactivation. These end points were not observed after irradiation with the selected NUV wavelengths or the broad spectrum solar-UV. Thus, neither broad spectrum solar-UV nor monochromatic NUV wavelengths resulted in the derepression of the recA promoter. Further, prior exposure of the cells either to the selected monochromatic NUV wavelengths or to solar-UV inhibited (a) the induction of beta-galactosidase by subsequent 254-nm radiation, (b) subsequent 254-nm induction of lambda prophage, (c) Weigle reactivation, and (d) mutation frequency. These observations are consistent with the hypothesis that NUV blocks subsequent recA protease action.
Mol Gen Genet 1984
PMID:Near-ultraviolet radiation blocks SOS responses to DNA damage in Escherichia coli. 622 13

The temperate bacteriophage Mu transduces the 4363 bp multi-copy plasmid pBR322 at frequencies similar to those of chromosomal markers. Plasmid transducing particles contain DNA molecules of Mu DNA length. Plasmid DNA is transduced as a head-to-tail oligomer that becomes circularized in the recipient cell. The rec system of the donor strain participates in oligomer formation and the rec system of the recipient strain is required for oligomer circularization. Possible mechanisms that may explain the origin of plasmid transducing particles are discussed.
Mol Gen Genet 1984
PMID:Transduction of multi-copy plasmid pBR322 by bacteriophage Mu. 623 67

Tn9 is a transposable element in which a gene (cat) determining chloramphenicol resistance is flanked by directly repeated sequences that are homologous to the insertion sequence IS1. We show here that infection of Escherichia coli K12 (under Rec-Red-Int- conditions) with a lambda bio transducing phage carrying Tn9 results in the formation of lambda bio transductants as frequently as cat transductants as frequently as cat transductants (about 1 per 10(6) to 10(7) infected cells). Most of the lambda bio transductants do not carry cat, just as most of the cat transductants do not carry lambda bio. In spite of the absence of cat, the lambda bio prophage can transpose a second time, from the E. coli chromosome to different sites on an F'gal plasmid. Analysis of the structure of the transposed lambda bio element, by restriction nuclease digestion and by electron microscopy, demonstrates that the integrated lambda bio prophage is flanked by directly repeated IS1 elements. We conclude that there is no genetic information for the ability to transpose encoded in the non-repeated portion of Tn9, i.e. that the directly repeated IS1 elements alone are responsible for Tn9 transposition.
Mol Gen Genet 1980 Apr
PMID:Transposition of IS1-lambdaBIO-IS1 from a bacteriophage lambda derivative carrying the IS1-cat-IS1 transposon (Tn9). 624 15

The recombination proficiency of three recipient strains of Escherichia coli K12 carrying different plasmids was investigated by conjugal mating with Hfr Cavalli. Some plasmids (e.g. R1drd 19, R6K) caused a marked reduction in the yield of recombinants formed in crosses with Hfr but did not reduce the ability of host strains to accept plasmid F104. The effect of plasmids on recombination was host-dependent. In Hfr crosses with AB1157 (R1-19) used as a recipient the linkage between selected and unselected proximal markers of the donor was sharply decreased. Plasmid R1-19 also decreased the yield of recombinants formed by recF, recL, and recB recC sbcA mutants, showed no effect on the recombination proficiency of recB recC sbcB mutant, and increased the recombination proficiency of recB, recB recC sbcB recF, and recB recC sbcB recL mutants. An ATP-dependent exonuclease activity was found in all tested recB recC mutants carrying plasmid R1-19, while this plasmid did not affect the activity of exonuclease I in strain AB1157 and its rec- derivatives. The same plasmid was also found to protect different rec- derivatives of the strain AB1157 against the lethal action of UV light. We suppose that a new ATP-dependent exonuclease determined by R1-19 plays a role in both repair and recombination of the host through the substitution of or competition with the exoV coded for by the genes recB and recC.
Mol Gen Genet 1980
PMID:Plasmid control of recombination of E. coli K12. 625 17

When Escherichia coli K12(lambda) lysogens are infected with heteroimmune lambda phage, which are unable to replicate, general recombination between phage and prophage depends on the bacterial recF gene. It has been shown that in E. coli K12 postconjugational recombination, the RecF pathway only works with full efficiency if exonuclease I is absent (Clark 1973). However, results presented in this paper indicate that under conditions in which lambda replication is blocked, the recombination pathway dependent on the recF gene is fully active in producing viral recombinants even, if the phage is Red+, in the presence of exonuclease I. In contrast, removal of lambda exonuclease and beta protein requires elimination of exonuclease I for an efficient RecF pathway. It is concluded that the Red system cooperates with the RecF pathway and that this cooperation involves overcoming the inhibitor effects of exonuclease I. In the absence of lambda exonuclease, beta protein stimulates recF-dependent recombination but does not suffice to prevent the negative effect of exonuclease I. In the presence of beta protein, full efficiency of the RecF pathway can be obtained either via cooperation with lambda exonuclease I or, if the viral exonuclease is defective, via inactivation of exonuclease I. Since activity of lambda exonuclease appears necessary to overcome the inhibitory effects of exonuclease I, it is proposed here that lambda exonuclease diverts material from the RecF pathway in a shunt reaction which allows completion of recF-initiated recombinational intermediates via a mechanism insensitive to exonuclease I. When lambda replication is allowed, the Rec system produces viral recombinants mainly via a recF-independent mechanism. However, a major contribution to the RecF pathway to lambda recombination is observed after removal of the Red system and exonuclease.
Mol Gen Genet 1981
PMID:Role of the recF gene of Escherichia coli K-12 in lambda recombination. 626 23

The effect of a large number of Tn3 insertions in the vir region of the Ti plasmid pTiA6NC on the virulence of Agrobacterium was determined. The Vir- insertions were mapped in three of the five loci that have been defined previously. Merodiploid Rec- strains carrying one insertion mutation on the Ti plasmid and another insertion mutation (or the homologous wild-type region) on a compatible plasmid were constructed and used in complementation tests for virulence in test plants. This analysis has revealed that there are ten units of gene expression, presumably transcription units in the vir region. Mutation in one of these units is confirmed to be dominant while those in all others are recessive. Co-infection of test plants with pairs of insertion mutants did not restore virulence.
Mol Gen Genet 1982
PMID:Units of genetic expression in the virulence region of a plant tumor-inducing plasmid of Agrobacterium tumefaciens. 629 72

Mutation of the uvrD gene of Escherichia coli is associated with an increased capacity for genetic recombination. The hyper-recombination effect is abolished by an additional mutation in lexA that limits synthesis of RecA protein and other gene products regulated by LexA repressor, and is not restored when increased synthesis of RecA protein is facilitated by a recAoc mutation. The viability of uvrD lexA strains is reduced and revertants selected on the basis of improved growth fall into three categories: those that are lexA+, or carry another mutation in lexA that directly suppresses the lexA defect; recA mutants that have lost the capacity for recombination altogether; and a third class which carry a mutation that is not in lexA or recA and which restores the hyper-rec phenotype but does not otherwise suppress the lexA defect. These results indicate that the hyper-recombination effect of a uvrD mutation is an induced response catalysed by RecA protein and at least one other lexA regulated activity.
Mol Gen Genet 1983
PMID:lexA dependent recombination in uvrD strains of Escherichia coli. 630 61

We describe a 4.5 kilobase transposon, Tn4001, which mediates resistance to gentamicin, tobramycin and kanamycin in Staphylococcus aureus. Originally detected in plasmid pSK1, Tn4001 was shown to undergo rec-independent transposition to the chromosome from this plasmid and from an inserted derivative of the plasmid pII147. Heteroduplexes between plasmids with and without Tn4001 demonstrated a characteristic stem and loop structure with inverted repeats of approx. 1.3 kilobases.
Mol Gen Genet 1984
PMID:Tn4001: a gentamicin and kanamycin resistance transposon in Staphylococcus aureus. 632 27

Specialized transducing phages rho 11spoIIC and phi 105spoIIC, carrying the Bacillus subtilis sporulation gene spoIIC, were constructed by the prophage transformation method. An EcoRI fragment (2.4 MDal) carrying the spoIIC gene was isolated from the phi 105spoIIC genome and recloned into the EcoRI site of plasmid pUB110. The recombinant plasmids corrected the sporulation defect of a Spo- Rec- host, but slightly inhibited the sporulation of a Spo+ Rec- host.
J Gen Microbiol 1984 Apr
PMID:Cloning of sporulation gene spoIIC in Bacillus subtilis. 633 Feb 86


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