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)

The mutagenesis in phage T7 after MMS-, HNO2-, hydroxylamine-, 5-BUdR-, and 2-AP-treatment in relation to host controlled functions is investigated. There was no dependence of the induction of mutations on the character of the host strains (rec, hcr). A back mutation system (amber system) and a forward mutation system (host range system) have been used. Substances which cause mainly transitions from GC to AT do not lead or only rarely lead to reversions of the amber system; but chemicals producing transitions from AT to GC do so.
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PMID:Mutagenesis in bacteriophage T7. I. Chemically induced mutagenesis. 78 28

Protoplast fusion between the Rec- mutant RN981 (L. Wyman, R. V. Goering, and R. P. Novick, Genetics 76:681-702, 1974) of Staphylococcus aureus NCTC 8325 and a Rec+ NCTC 8325 derivative yielded Rec+ recombinants that exhibited the increased sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine characteristic of RN981. Transformation analyses identified a specific mutation, designated ngr-374, that was responsible not only for N-methyl-N'-nitro-N-nitrosoguanidine sensitivity, but also sensitivity to methyl methanesulfonate, ethyl methanesulfonate, nitrous acid, and UV irradiation. However, ngr-374-carrying recombinants showed no significant increase in their sensitivity to mitomycin C or 4-nitroquinoline 1-oxide and were unaffected in recombination proficiency. In vitro assays showed that ngr-374-carrying strains had lower apurinic/apyrimidinic endonuclease activities than the wild type. The chromosomal locus occupied by ngr-374 was shown to exist in the gene order omega(Chr::Tn551)40-ngr-374-thrB106.
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PMID:Characterization and genetic mapping of a mutation affecting apurinic endonuclease activity in Staphylococcus aureus. 243 Sep 40

Recombinant plasmids containing the recA gene from Pseudomonas aeruginosa were used in complementation, transcriptional, and translational studies to examine the nature of rec-102 and rec-2, mutations which confer a recA-like mutant phenotype on P. aeruginosa PAO strains. For comparison, recA7::Tn501 mutants of strain PAO were constructed by gene replacement. The rec-2 and rec-102 alleles were shown to be recA alleles; plasmids containing the recA gene complemented the three rec mutant strains for defects associated with recA mutation. Northern blot analyses indicated that the recA gene in P. aeruginosa was transcribed as two distinct mRNAs of approximately 1.2 and 1.4 kilobases (kb). A plasmid encoding both transcripts of recA complemented all defects associated with the three recA mutations rec-2, rec-102, and recA7. However, a 2.4-kb subclone (pJH13) encoding only the smaller transcript of the recA gene was expressed differently in the three recA allele backgrounds and served as a tool to distinguish the nature of the rec-2 and rec-102 mutations in recA. A minicell analysis showed that a plasmid expressing both of the recA gene transcripts or one that expressed only the smaller transcript both produced the same 42-kilodalton recA protein. A chloramphenicol acetyltransferase gene fusion in the 3' end of the recA transcript showed that the recA gene of P. aeruginosa was induced following treatment with a DNA-damaging agent (methyl methanesulfonate). The recA7 mutant constructed here showed no recA-related transcript or protein under inducing conditions, and pJH13 in this host produced only low levels of the smaller recA transcript and low levels of recA protein. The rec-2 mutant produced a detectable transcript but no recA protein following induction. The presence of low levels of activated recA protein encoded by pJH13 in the rec-2 mutant resulted in wild-type transcriptional levels of chromosomally encoded recA, but no recA protein was detectable. Thus, the rec-2 allele of recA was normal with respect to induction of mRNA, but these transcripts were defective in either translation or synthesis of a stable protein. The rec-102 mutant also produced a detectable transcript and no recA protein following induction, but having pJH13 in the cell to produce low levels of activated recA protein resulted in overproduction of chromosomally encoded recA transcripts and active recA protein. Thus, the recA defect in the rec-102 mutant is apparently in the interaction between recA and a lexA-like repressor.
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PMID:Transcriptional and translational analyses of recA mutant alleles in Pseudomonas aeruginosa. 245 Aug 68

Mutations were induced in Neurospora which cause increased sensitivity to MMS (methyl methane-sulfonate) and other mutagens. Genetic analysis of such mus demonstrated that some of them defined new DNA repair genes (mus-21, and mus-27 to mus-30), while others represented new alleles in previously known genes. To characterize them further, and especially to identify rec- types which have not yet been found in this species, many MMS-sensitive strains were tested for cross-sensitivities to bleomycin (BLM) and to hydrogen peroxide (H2O2) to which some rec- of other species are hypersensitive. In Neurospora, many of the MMS-sensitive mutants were found to be cross-sensitive to BLM and frequently these were also hypersensitive to ionizing radiation. Bleomycin sensitivity was demonstrated for all alleles of 10 different genes, 4 of them new ones, with mus-27 being the most sensitive of the latter (resembling uvs-6; Koga and Schroeder, 1987, Mutation Res., 183, 139). In contrast, very few of the MMS-sensitive mutants were hypersensitive to H2O2 and, in general, results of H2O2 tests were variable and differences between strains small. However, consistent deviations from wild type were observed in a few cases (most clearly for mus-9 and mus-11) when results from treatments of germinating conidia were compared with those of non-growing ones.
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PMID:Sensitivity to bleomycin and hydrogen peroxide of DNA repair-defective mutants in Neurospora crassa. 246 86

The Haemophilus influenzae Rd rec-1+ gene was cloned from a partial chromosomal digest into a plasmid vector as a 20-kilobase-pair (kbp) BstEII fragment and then subcloned. The smallest subclone with rec-1+ activity carried a 3.1-kbp EcoRI fragment. The identity of the rec-I gene in these clones was confirmed by transforming an Rd strain carrying a leaky rec-1 mutation (recA4) to resistance to methyl methanesulfonate (MMS) by using whole or digested plasmids. It was demonstrated that the Rec+ phenotype of the MMSr transformants was linked to the strA, novAB, and mmsA loci, as expected if the recA4 allele had been replaced by rec-1+. In growing cultures (rec-1 or rec+), all rec-1+-carrying plasmids induced near-maximal levels of transformability when their hosts reached stationary phase; these levels are 100 to 1,000 times higher than the values seen with strains not carrying a Rec plasmid. Transfer of the 3.1-kbp subclone was greatly reduced compared with transfer of similarly sized vector plasmids, and the resulting transformants grew slowly; this suggests an explanation of my failure to directly clone this fragment from chromosomal DNA digests. Transfer of a rec-1+ plasmid to a very poorly genetically transformable H. influenzae Rb strain resulted in greatly increased transformability. Transfer of such plasmids to a noncompetent H. influenzae Rc strain did not render this strain competent. It is suggested that transformability of Rd and Rb strains is limited by rec-1 expression but that the noncompetence of Rc has some other basis.
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PMID:Cloning and characterization of the Haemophilus influenzae Rd rec-1+ gene. 278 90

We cloned a 2.3-kilobase-pair fragment of the Pseudomonas aeruginosa PAO chromosome which is capable of complementing recA mutations of Escherichia coli. The recA-complementing activity was further localized to a 1.5-kilobase-pair PvuII-HindIII fragment. Southern blot analysis under conditions of high stringency indicated that DNA sequence homology is shared by the E. coli recA gene and the P. aeruginosa recA analog. The cloned recA analog was shown to restore resistance to methyl methanesulfonate, nitrofurantoin, and UV irradiation to E. coli recA mutants. Upon introduction of the cloned P. aeruginosa gene, these mutants regained recombination proficiency in HfrH-mediated conjugation and the ability to induce lambda prophages and SOS functions (din gene transcription) after exposure to DNA-damaging agents. Lambda prophage carrying a cI ind mutation was not inducible, suggesting that the mechanism of induction of these SOS functions by the P. aeruginosa RecA analog is similar to that by the activated E. coli RecA protein. The product of the recA analog was identified in minicells as a protein of approximately 47,000 daltons. Western blot analysis using anti-E. coli RecA antibody demonstrated that this protein is antigenically cross-reactive with the E. coli recA protein. The recA-containing fragment was cloned into the broad-host-range vector pCP13 and introduced into Rec- strains of P. aeruginosa containing the rec-102 allele. The plasmid was shown to restore recombination proficiency in FP5-mediated conjugations and to restore resistance to UV irradiation and methyl methanesulfonate to these Rec- mutants. It was shown that a wild-type allele of rec-102 is necessary for UV-mediated induction of D3 and F116 prophages. The cloned recA analog restored the UV inducibility of these prophages in rec-102 mutants. These data indicate that rec-102 is a mutant allele of the P. aeruginosa recA gene and suggest that there has been considerable conservation of the recA gene in the evolution of the gram-negative bacteria.
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PMID:Characterization of the Pseudomonas aeruginosa recA analog and its protein product: rec-102 is a mutant allele of the P. aeruginosa PAO recA gene. 303 Oct 14

DNA lesions may be recognized and repaired by more than one DNA-repair process. If two repair systems with different error frequencies have overlapping lesion specificity and one or both is inducible, the resulting variable competition for the lesions can change the biological consequences of these lesions. This concept was demonstrated by observing mutation in yeast cells (Saccharomyces cerevisiae) exposed to combinations of mutagens under conditions which influenced the induction of error-free recombinational repair or error-prone repair. Total mutation frequency was reduced in a manner proportional to the dose of 60Co-gamma- or 254 nm UV radiation delivered prior to or subsequent to an MNNG exposure. Suppression was greater per unit radiation dose in cells gamma-irradiated in O2 as compared to N2. A rad3 (excision-repair) mutant gave results similar to wild-type but mutation in a rad52 (rec-) mutant exposed to MNNG was not suppressed by radiation. Protein-synthesis inhibition with heat shock or cycloheximide indicated that it was the mutation due to MNNG and not that due to radiation which had changed. These results indicate that MNNG lesions are recognized by both the recombinational repair system and the inducible error-prone system, but that gamma-radiation induction of error-free recombinational repair resulted in increased competition for the lesions, thereby reducing mutation. Similarly, gamma-radiation exposure resulted in a radiation dose-dependent reduction in mutation due to MNU, EMS, ENU and 8-MOP + UVA, but no reduction in mutation due to MMS. These results suggest that the number of mutational MMS lesions recognizable by the recombinational repair system must be very small relative to those produced by the other agents. MNNG induction of the inducible error-prone systems however, did not alter mutation frequencies due to ENU or MMS exposure but, in contrast to radiation, increased the mutagenic effectiveness of EMS. These experiments demonstrate that in this lower eukaryote, mutagen exposure does not necessarily result in a fixed risk of mutation, but that the risk can be markedly influenced by a variety of external stimuli including heat shock or exposure to other mutagens.
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PMID:Inducible DNA-repair systems in yeast: competition for lesions. 354 7

The in vivo repair processes of Alteromonas espejiana, the host for bacteriophage PM2, were characterized, and UV- and methyl methanesulfonate (MMS)-sensitive mutants were isolated. Wild-type A. espejiana cells were capable of photoreactivation, excision, recombination, and inducible repair. There was no detectable pyrimidine dimer-DNA N-glycosylase activity, and pyrimidine dimer removal appeared to occur by a pathway analogous to the Escherichia coli Uvr pathway. The UV- and MMS-sensitive mutants of A. espejiana included three groups, each containing at least one mutation involved with excision, recombination, or inducible repair. One group that was UV sensitive but not sensitive to MMS or X rays showed a decreased ability to excise pyrimidine dimers. Mutants in this group were also sensitive to psoralen plus near-UV light and were phenotypically analogous to the E. coli uvr mutants. A second group was UV and MMS sensitive but not sensitive to X rays and appeared to contain mutations in a gene(s) involved in recombination repair. These recombination-deficient mutants differed from the E. coli rec mutants, which are MMS and X-ray sensitive. The third group of A. espejiana mutants was sensitive to UV, MMS, and X rays. These mutants were recombination deficient, lacked inducible repair, and were phenotypically similar to E. coli recA mutants.
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PMID:Repair-defective mutants of Alteromonas espejiana, the host for bacteriophage PM2. 669 49

The Escherichia coli helD (encoding helicase IV) and uvrD (encoding helicase II) genes have been deleted, independently and in combination, from the chromosome and replaced with genes encoding antibiotic resistance. Each deletion was verified by Southern blots, and the location of each deletion was confirmed by P1-mediated transduction. Cell strains containing the single and double deletions were viable, indicating that helicases II and IV are not essential for viability. Cell strains lacking helicase IV (delta helD) exhibited no increase in sensitivity to UV irradiation but were slightly more resistant to methyl methanesulfonate (MMS) than the isogenic wild-type cell strain. As expected, cell strains containing the helicase II deletion (delta uvrD) were sensitive to both UV irradiation and MMS. The introduction of the helicase IV deletion into a delta uvrD background had essentially no effect on the UV and MMS sensitivity of the cell strains analyzed. The double deletions, however, conferred a Rec- mutant phenotype for conjugational and transductional recombination in both recBC sbcB(C) and recBC sbcA backgrounds. The Rec- mutant phenotype was more profound in the recBC sbcB(C) background than in the recBC sbcA background. The recombination-deficient phenotype indicates the direct involvement of helicase II and/or helicase IV in the RecF pathway [recBC sbcB(C) background] and RecE pathway (recBC sbcA background) of recombination. The modest decrease in the recombination frequency observed in single-deletion mutants in the recBC sbcB(C) background suggests that either helicase is sufficient. In addition, helicase IV has been overexpressed in a tightly regulated system. The data suggest that even modest overexpression of helicase IV is lethal to the cell.
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PMID:Double helicase II (uvrD)-helicase IV (helD) deletion mutants are defective in the recombination pathways of Escherichia coli. 833 23

The B. subtilis DeltahelD allele rendered cells proficient in transformational recombination and moderately sensitive to methyl methanesulfonate when present in an otherwise Rec(+) strain. The DeltahelD allele was introduced into rec-deficient strains representative of the alpha (recF strain), beta (addA addB), gamma (recH), epsilon (DeltarecU), and zeta (DeltarecS) epistatic groups. The DeltahelD mutation increased the sensitivity to DNA-damaging agents of addAB, DeltarecU, and DeltarecS cells, did not affect the survival of recH cells, and decreased the sensitivity of recF cells. DeltahelD also partially suppressed the DNA repair phenotype of other mutations classified within the alpha epistatic group, namely the recL, DeltarecO, and recR mutations. The DeltahelD allele marginally reduced plasmid transformation (three- to sevenfold) of mutations classified within the alpha, beta, and gamma epistatic groups. Altogether, these data indicate that the loss of helicase IV might stabilize recombination repair intermediates formed in the absence of recFLOR and render recFLOR, addAB, and recH cells impaired in plasmid transformation.
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PMID:Genetic recombination in Bacillus subtilis 168: effect of DeltahelD on DNA repair and homologous recombination. 1154 44


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