Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A persistently reduced cloning efficiency occurs in many of the cloned progeny of Chinese hamster ovary (CHO) cells surviving X irradiation, a stable phenotype we have previously termed delayed reproductive death (Int. J. Radiat. Biol. 60, 483-496, 1991). We now report that this phenotype is also induced by the alkylating agent ethyl methanesulfonate (EMS), but not by irradiation with ultraviolet light. The restriction endonuclease HinfI, which binds at G [symbol: see text] ANTC DNA sequences and generates cohesive-end double-strand breaks, was also efficient in inducing delayed reproductive death. On the other hand, an X-ray-sensitive CHO mutant, xrs-5, which is defective in the repair of DNA double-strand breaks, did not show this phenotype following X irradiation. These results suggest that DNA double-strand breaks, as well as the endogenous repair processes for these breaks, are associated with the induction of the delayed reproductive death phenotype in CHO cells. The possible mechanism for the induction of delayed reproductive death by EMS is discussed.
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PMID:Evidence that DNA double-strand breaks initiate the phenotype of delayed reproductive death in Chinese hamster ovary cells. 162 49

EcoRI restriction endonuclease (RE), which produces cohesive-ended double-strand breaks (dsb) in DNA, was tested in the ethyl methanesulfonate- and X-ray-sensitive CHO mutant EM9 and its parental cell strain AA8 for its chromosomal aberration-inducing effect. The RE was efficiently introduced by electroporation into AA8 cells, while the mutant cells showed a very high sensitivity to electroporation, which consistently resulted in cell death. Nevertheless, the incubation of EM9 cells in the presence of EcoRI, without electroporation, was sufficient to induce about three times the chromosome damage observed in the electroporated parental cell line AA8 for any given dose of the RE.
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PMID:Induction of chromosomal aberrations in the CHO mutant EM9 and its parental line AA8 by EcoRI restriction endonuclease: electroporation experiments. 198 65

Cosmid cloning and mutagenesis were used to identify genes involved in the production of phaseolotoxin, the chlorosis-inducing phytotoxin of Pseudomonas syringae pv. phaseolicola, the causal agent of halo blight of bean (Phaseolus vulgaris L.). Eight stable clones were isolated from a genomic cosmid library by en masse mating to 10 ethyl methanesulfonate (EMS)-induced Tox- mutants. In cross-matings, each suppressed all 10 mutants as well as an additional 70 EMS-induced Tox- mutants (and one UV-induced Tox- mutant). On the basis of restriction endonuclease analysis and hybridization studies, the clones were grouped into three classes. Clones in a particular class shared common fragments, whereas clones in different classes did not. Clones from class I (but not classes II and III) also suppressed Tn5-induced Tox- mutants. Interposon mutagenesis and marker exchange of a representative clone from class III into the wild-type genome did not alter its Tox+ phenotype, indicating that this clone does not harbor structural or regulatory genes involved in phaseolotoxin production. We suggest that the genome of P. syringae pv. phaseolicola contains a "hot spot" in one of the functions involved in toxin production which is affected by EMS and UV and that heterologous clones are able to suppress the Tox- phenotype because their inserts encode products that are able to substitute for the product of the mutated gene. Alternatively, the inserts may contain sequences which titrate a repressor protein. In either case, the data suggest that suppression of EMS- and UV-induced mutants occurs when heterologous clones are present in multiple copies.
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PMID:Pseudomonas syringae pv. phaseolicola genomic clones harboring heterologous DNA sequences suppress the same phaseolotoxin-deficient mutants. 199 9

We describe the cloning and function of the human XRCC1 gene, which is the first mammalian gene isolated that affects cellular sensitivity to ionizing radiation. The CHO mutant EM9 has 10-fold-higher sensitivity to ethyl methanesulfonate, 1.8-fold-higher sensitivity to ionizing radiation, a reduced capacity to rejoin single-strand DNA breaks, and a 10-fold-elevated level of sister chromatid exchange compared with the CHO parental cells. The complementing human gene was cloned from a cosmid library of a tertiary transformant. Two cosmid clones produced transformants that showed approximately 100% correction of the repair defect in EM9 cells, as determined by the kinetics of strand break repair, cell survival, and the level of sister chromatid exchange. A nearly full-length clone obtained from the pcD2 human cDNA expression library gave approximately 80% correction of EM9, as determined by the level of sister chromatid exchange. Based on an analysis of the nucleotide sequence of the cDNA insert compared with that of the 5' end of the gene from a cosmid clone, the cDNA clone appeared to be missing approximately 100 bp of transcribed sequence, including 26 nucleotides of coding sequence. The cDNA probe detected a single transcript of approximately 2.2 kb in HeLa polyadenylated RNA by Northern (RNA) blot hybridization. From the open reading frame and the positions of likely start sites for transcription and translation, the size of the putative XRCC1 protein is 633 amino acids (69.5 kDa). The size of the XRCC1 gene is 33 kb, as determined by localizing the endpoints on a restriction endonuclease site map of one cosmid clone. The deduced amino acid sequence did not show significant homology with any protein in the protein sequence data bases examined.
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PMID:Molecular cloning of the human XRCC1 gene, which corrects defective DNA strand break repair and sister chromatid exchange. 224 54

A single plasmid of 55 kilobases was found in crude cell lysates of each of nine strains of Rhodospirillum rubrum. Restriction endonuclease analysis showed identical fragment patterns with a given nuclease for all plasmids except one, for which an additional EcoRI site was observed. Elimination of the plasmid required that the cells be passaged several times in 25 mM calcium-containing medium, followed by at least two passages under photosynthetic growth conditions in low-calcium medium before treatment with ethyl methanesulfonate. The resulting plasmidless mutants only grew aerobically and were all incapable of pigment formation and photosynthetic growth, suggesting that plasmid DNA is required for photosynthetic competence in R. rubrum.
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PMID:Characterization of a Rhodospirillum rubrum plasmid: loss of photosynthetic growth in plasmidless strains. 631 17

Mucoid strains of Pseudomonas aeruginosa isolated from the sputum of cystic fibrosis patients produce copious quantities of an exopolysaccharide known as alginic acid. Since clinical isolates of the mucoid variants are unstable with respect to alginate synthesis and revert spontaneously to the more typical nonmucoid phenotype, it has been difficult to isolate individual structural gene mutants defective in alginate synthesis. The cloning of the genes controlling alginate synthesis has been facilitated by the isolation of a stable alginate-producing strain, 8830. The stable mucoid strain was mutagenized with ethyl methanesulfonate to obtain various mutants defective in alginate biosynthesis. Several nonmucoid (Alg-) mutants were isolated. A mucoid P. aeruginosa gene library was then constructed, using a cosmid cloning vector. DNA isolated from the stable mucoid strain 8830 was partially digested with the restriction endonuclease HindIII and ligated to the HindIII site of the broad host range cosmid vector, pCP13. After packaging in lambda particles, the recombinant DNA was introduced via transfection into Escherichia coli AC80. The clone bank was mated (en masse) from E. coli into various P. aeruginosa 8830 nonmucoid mutants with the help of pRK2013, which provided donor functions in trans, and tetracycline-resistant exconjugants were screened for the ability to form mucoid colonies. Three recombinant plasmids, pAD1, pAD2, and pAD3, containing DNA inserts of 20, 9.5, and 6.2 kilobases, respectively, were isolated based on their ability to restore alginate synthesis in various strain 8830 nonmucoid (Alg-) mutants. Mutants have been assigned to at least four complementation groups, based on complementation by pAD1, pAD2, or pAD3 or by none of them. Introduction of pAD1 into the spontaneous nonmucoid strain 8822, as well as into other nonmucoid laboratory strains of P. aeruginosa such as PAO and SB1, was found to slowly induce alginate synthesis. This alginate-inducing ability was found to reside on a 7.5-kilobase EcoRI fragment that complemented the alg-22 mutation of strain 8852. The pAD1 chromosomal insert which complements the alg-22 mutation was subsequently mapped at ca. 19 min of the P. aeruginosa PAO chromosome.
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PMID:Cloning of genes controlling alginate biosynthesis from a mucoid cystic fibrosis isolate of Pseudomonas aeruginosa. 633 52

Ethyl methanesulfonate rendered a high percentage of Rhodospirillum rubrum cells plasmidless and photosynthetically incompetent (Kuhl et al., J. Bacteriol. 156:737-742, 1983). By probing restriction endonuclease-digested chromosomal DNA from these plasmidless strains with 32P-labeled R. rubrum plasmid DNA, we showed that no homology exists between the plasmid and the chromosomal DNA of the mutant. Loss of the plasmid in all the nonphotosynthetic isolates was accompanied by the synthesis of spirilloxanthin under aerobic growth conditions, resistance to cycloserine and HgCl2, and loss of ability to grow fermentatively on fructose. Changes in both the protein and lipid composition of the membranes and the impaired uptake of 203HgCl2 in the plasmidless strains (compared with the wild type) suggest either that membrane modification occurs as a result of plasmid loss, accounting for several of the acquired phenotype characteristics of the cured strains, or that both membrane modification and plasmid loss are part of the same pleiotropic mutation.
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PMID:Plasmidless, photosynthetically incompetent mutants of Rhodospirillum rubrum. 643 14

A study of the apurinic/apyrimidinic (AP) endonuclease activities of a mutant line of CHO cells, EM9, and its parental cell line, AA8, was undertaken to determine if the defective DNA repair exhibited by the mutant cell line after exposure to ethyl methanesulfonate was due to a defective AP endonuclease activity. Phosphocellulose chromatography of cell extracts resolved the AP endonuclease activities of both cell lines into two peaks as seen previously in mouse and human cells. No difference was found between the mutant and parental cell lines in the relative amount of AP endonuclease activity present in the two peaks.
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PMID:Apurinic/apyrimidinic endonuclease activities appear normal in the CHO-cell ethyl methanesulfonate-sensitive mutant, EM9. 648 94

Eighteen EMS-induced mutant strains of S. cerevisiae with increased sensitivity to petite induction by sulfanilamide-aminopterin treatment have been isolated. Four of these strains demonstrated a concomitant increase in sensitivity to the petite-inducing effects of u.v. irradiation and of growth at an elevated temperature. Of these, two were shown to be a consequence of recessive nuclear mutations at one gene (sas1-1 and sas1-2). Expression of the two remaining mutations was too low to permit genetic analysis. All three petite-inducing treatments used in this study are known to reduce the hydrogen bond strength between the two strands of double stranded DNA, and the existence of multiple sensitivity is discussed in terms of an alteration of a mitochondrial endonuclease which acts preferentially at sites of reduced attraction.
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PMID:Nuclear mutations in Saccharomyces cerevisiae conferring multiple sensitivity to petite-inducing treatments. 676 51

The number of apurinic/apyrimidinic (AP) sites in supercoiled SV40 deoxyribonucleic acid (DNA) after treatment with several electrophilic mutagens was quantitated by electrophoretic analysis of the DNA after cleavage of the phosphodiester bonds adjacent to AP sites by a specific endonuclease. The compounds studied, in order of increasing yields of AP sites obtained on incubation with the DNA for 5 h at 37 degrees C, were dimethylcarbamoyl chloride, ethyl methanesulfonate, N-ethyl-N-nitrosourea, 2-(N-acetoxyacetylamino)fluorene, beta-propiolactone, N-methyl-N-nitrosourea, methyl methanesulfonate, 1'-acetoxyestragole, 4-(N-acetoxyacetylamino)stilbene, (+/-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene, N-(benzoyloxy)-N-methyl-4-aminoazobenzene, and 1-pyrenyloxirane. After a 5-h incubation at 37 degrees C and extraction of unreacted compound, further incubation at 70 degrees C generally increased the yield of AP sites; an exception was N-(benzoyloxy)-N-methyl-4-aminoazobenzene-reacted DNA. Except for DNA treated with N-ethyl-N-nitrosourea and N-methyl-N-nitrosourea, which are known to bind to a significant extent to DNA phosphates, the number of alkali-labile lesions in the treated DNA was similar to the number of AP sites. For the compounds studied there was no direct correlation between the number of AP sites produced and missense mutagenic activity, as measured in Salmonella typhimurium strain TA100.
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PMID:Estimation of apurinic/apyrimidinic sites and phosphotriesters in deoxyribonucleic acid treated with electrophilic carcinogens and mutagens. 677 63


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