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)

Intravenous administration of lead acetate to rabbits for 10 weeks at 2 week intervals resulted in significantly elevated blood lead levels, slight anemia with marked microspherocytosis and moderate basophilic stippling, and marked depression of red cell delta-aminolevulinic acid (ALA) dehydratase activity. However the decrease in red cell pyrimidine 5'-nucleotidase (P5N) activity was slight when compared to the red cell P5N activity of comparable reticulocyte-rich blood, and intracellular accumulation of pyrimidine nucleotides could not be demonstrated. In the in vitro inhibition test the same degree of inhibition of red cell P5N activity seen in hereditary red cell P5N deficiency was obtained by using a lead concentration 200--400 times higher than the lead levels detected in human plumbism. Most importantly, there were no differences in the lead-induced inhibition of human and rabbit red cell P5N. From the results of the in vitro inhibition test, lead-induced red cell P5N deficiency appears to be one of several pathogenic mechanisms in chronic lead exposure associated with the accumulation of lead in bone marrow. A decrease in rec cell P5N activity could not be demonstrated despite the marked depression in red cell ALA dehydratase activity, and slight anemia with marked microspherocytosis and moderate basophilic stippling in this experiment. These results suggest that lead affects red cells at multiple metabolic loci.
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PMID:A role of red cell pyrimidine 5'-nucleotidase in experimental lead poisoning. 23 20

Upon exposure to the carcinogens N-acetoxy-N-2-acetylaminofluorene and 7-bromomethyl-benz[a]anthracene, which bind covalently to DNA, ether-permeabilized (nucleotide-permeable) Escherichia coli wild-type cells responded with DNA excision repair. This repair was missing in mutants carrying defects in genes uvrA, uvrB and uvrC, whereas it was present in uvrD and several rec mutants. Enzymic activities involved were identified by measuring repair polymerization and size reduction of denatured DNA. 1. An easily measurable effect in E. coli wild-type cells was carcinogen-induced repair polymerization. When initiated by N-acetoxy-N-2-acetylaminofluorene or 7-bromomethyl-benz[a]anthracene, it depended upon an ATP-requiring step; CTP, GTP or UTP did not substitute for ATP. DNA repair synthesis was inhibited by p-chloromercuribenzoate and quinacrine. In uvrA, uvrB and uvrC mutants no carcinogen-stimulated DNA synthesis could be detected, indicating that steps involved in pyrimidine dimer excision are also involved in chemorepair. In recA, recB and recC mutant cells, repair synthesis was stimulated by the carcinogens to a normal extent. This evidence excludes the ATP-dependent recB,C deoxyribonuclease and recA gene products as playing an important role in carcinogen-induced excision repair. polA1 cells showed drastically reduced levels of rapair polymerization, indicating that DNA polymerase I is the main polymerizing enzyme. 2. As determined by DNA size reduction in alkaline sucrose gradients, the arylalkylating carcinogens caused endonucleolytic cleavage of endogenous DNA in wild-type cells. This incision step was most effectively performed in the presence of ATP; UTP, CTP and GTP were only slightly effective. Incision was inhibited by p-chloromercuribenzoate and quinacrine. When exposed to the arylalkylating carcinogens, uvrA, uvrB and uvrC mutant cells did not perform the incision step in the presence of ATP, suggesting the involvement of the respective gene products in the initiation of chemorepair.
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PMID:Carcinogen-induced DNA repair in nucleotide-permeable Escherichia coli cells. Analysis of DNA repair induced by the carcinogens N-acetoxy-N-2-acetylaminofluorene and 7-bromomethyl-benz(a)anthracene. 76 31

UV-induced pyrimidine dimers were excised from the DNA of wild-type and four mutant strains of Ustilago maydis. Excision was partially dose dependent. The kinetics of excision differed in recombination deficient strains (rec 1 and rec 2) from those found in a recombination proficient radiation-sensitive strain (uvs 3). At fluences above 100 J-m-2 excision was saturated in uvs 3 but not in rec 1 or rec 2. Fluences above 300 J-m-2 started to saturate excision in wild-type. pol1-1, a temperature-sensitive DNA polymerase mutant, was excision proficient at both the permissive (22 degree) and restrictive (32 degree) temperatures. Wild-type cells were observed to excise CC before CT or TT in high dose experiments.
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PMID:The excision of pyrimidine dimers from the DNA of mutant and wild-type strains of Ustilago. 115 59

A 713-base-pair Hae III fragment from bacteriophage T4 encompassing the denV gene with its preceding promoter has been cloned in a pBR322-derived positive-selection vector and introduced into a variety of DNA repair-deficient uvr and rec and uvr,rec Escherichia coli strains. The denV gene was found to be expressed, probably from its own promoter, causing pyrimidine dimer incision-deficient uvrA, uvrB, uvrC strains to be rescued by the denV gene. A uvrD (DNA helicase II) strain was also complemented, but to a lesser extent. A wild-type strain did not seem to be affected at the UV doses tested. Surprisingly, all recA, recB, and recC strains tested also showed an increased UV resistance, perhaps by reinforcement of the intact uvr system in these strains. Complementation of denV- T4 strains and host-cell reactivation of lambda phage was also observed in denV+ E. coli strains. Equilibrium sedimentation showed that DNA repair synthesis occurred in a UV-irradiated uvrA E. coli strain carrying the cloned denV gene. Southern blotting confirmed our earlier results [Valerie, K., Henderson, E. E. & de Riel, J. K. (1984) Nucleic Acids Res. 12, 8085-8096] that the denV gene is located at 64 kilobases on the T4 map. Phage T2 (denV-) did not hybridize to a denV-specific probe.
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PMID:Expression of a cloned denV gene of bacteriophage T4 in Escherichia coli. 299 91

Rat adrenocortical cells are almost completely dependent upon the continuous supply of cholesterol derived from serum lipoproteins. However, a prolonged (5-day) administration of 4-aminopyrazolo-pyrimidine (4-APP), a potent hypocholesterolaemic drug, though provoking a notable decrease in the intra-adrenal concentration of esterified and free cholesterol, did not significantly affect basal plasma level of corticosterone. Morphometry showed a conspicuous hypertrophy of zona fasciculata cells, coupled with a striking proliferation of smooth endoplasmic reticulum (SER) and peroxisomes and with a profound lipid-droplet depletion. The secretory response of zona fasciculata cells to ACTH was still present, but reduced by half with respect to control rats. The simultaneous administration of mevinolin, an inhibitor of cholesterol synthesis, to 4-APP-treated rats caused an additional drop in the intracellular content of free cholesterol and notably lowered basal plasma corticosterone concentration. Mevinolin magnified the 4-APP-induced zona fasciculata cell hypertrophy, as well as SER and peroxisome proliferation. The secretory response to ACTH was completely suppressed. These data are compatible with the view that the morphological changes, which rat zona fasciculata cells undergo during prolonged hypocholesterolaemia, are the expression of the activation of the endogenous cholesterol synthesis. This compensatory response, enabling zona fasciculata cells to maintain a normal basal rate of hormonal output and to respond (though less efficiently) to their main physiological stimulus, seems to be completely independent of any activation of the hypothalamo-hyphophyseal axis, since dexamethasone/ACTH treated rats were used. The hypothesis is advanced that the mechanism underlying this response may involve the decrease of the intracellular free-cholesterol pool.
Anat Rec 1988 Jul
PMID:Effects of mevinolin, an inhibitor of cholesterol synthesis, on the morphological and functional responses of rat adrenal zona fasciculata to a prolonged treatment with 4-aminopyrazolo-pyrimidine. 318 65

Strains of Escherichia coli that carry the mutation uvrA6 show no measurable excision of pyrimidine dimers and are easily killed by ultraviolet (UV) light, whereas strains that carry recA13 are defective in genetic recombination and are also UV-sensitive. An Hfr strain carrying uvrA6 was crossed with an F(-) strain carrying recA13. Among the recombinants identified, one carrying uvrA recA proved to be of exceptional sensitivity to UV light. It is estimated from the UV dose (0.2 erg/mm(2) at 253.7 nm) required to reduce the number of colony-forming cells by one natural logarithm that about 1.3 pyrimidine dimers were formed in a genome of 5 x 10(6) base pairs for each lethal event. This double mutant is 40 times more UV-sensitive than the excision-defective strain carrying uvrA6. The replication of one pyrimidine dimer is generally a lethal event in strains carrying recA13. Spontaneous breakdown and UV-induced breakdown of the deoxyribonucleic acid (DNA) of cells of the various genotypes were estimated by growing the cells in medium containing (3)H-thymidine and measuring both acid-precipitable and acid-soluble radioactivity. The UV-induced degradation in strains with recA13 did not require the uvr(+) genes and hence appears to depend upon a mechanism other than dimer excision. The greater level of survival after irradiation in Rec(+) as compared to Rec(-) bacteria may be due to a recovery mechanism involving the reconstruction of the bacterial chromosome through genetic exchanges which occur between the newly replicated sister duplexes and which effectively circumvent the damaged bases remaining in the DNA.
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PMID:Some properties of excision-defective recombination-deficient mutants of Escherichia coli K-12. 488 1

The uvr mutations of Escherichia coli K-12 decrease the ability of cells to survive ultraviolet light (UV), to excise pyrimidine dimers from their deoxyribonucleic acid and to reactivate bacteriophage exposed to UV. The rec mutations decrease the ability of the cells to survive UV and to undergo genetic recombination. Certain rec mutations, including recA1, rec-12, recA13, and rec-56, are necessary for the expression of liquid-holding recovery (LHR), observed as an increase in colony-forming ability when irradiated cells are held in buffer in the dark. These rec mutations appear to act indirectly to permit the detection of LHR rather than to affect its occurrence directly. We have tested the effect of uvr markers on LHR in cells containing one of these rec mutations. Recombinants containing rec-56 together with a uvr marker were constructed and tested for LHR. None of the 39 recombinants examined, carrying uvrA6, uvrB5, or uvrC34, showed LHR. Three rec(-)uvr(-) strains were also tested for photoreactivation. In all three, photoreactivation was observed, indicating that they contained detectable amounts of pyrimidine dimers. Our results are consistent with the idea that uvr mutations inactivate LHR, and suggest that LHR reflects excision-dependent repair of pyrimidine dimers.
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PMID:Dark recovery processes in Escherichia coli irradiated with ultraviolet light. II. Effect of uvr genes on liquid holding recovery. 488 4

Eight recombination-deficient (Rec(-)) mutants of Escherichia coli were studied. Progeny lines were obtained on solid media, by means of micromanipulation, and the colony-forming ability of individual cells was analyzed. Cells of all eight strains gave rise to colony-forming as well as non-colony-forming descendants ("lethal sectoring"). Lethal sectors, i.e., groups of non-colony-forming cells which originate from a common ancestor, appeared with frequencies per generation ranging between 4 and 20% in Rec(-) strains, whereas lethal sectors were rare in Rec(+) strains (less than 1%). A strain carrying a mutation (uvrA6) in one of the genes involved in pyrimidine dimer excision from deoxyribonucleic acid (DNA) showed twice as many lethal sectors per generation as a strain with the genotype uvrA(+). Similarly, a double mutant (AB2480, uvrA6, recA13) showed twice as much spontaneous lethal sectoring as the corresponding Rec(-) strain (uvrA(+), recA13). The kinetics of growth curves obtained in nutrient broth and the frequency of non-colony-forming units in stationary-phase broth cultures indicate clearly that lethal sectors occur in liquid cultures too. The causes for spontaneous lethal sectoring are unknown at present. It seems reasonable to assume that gene uvrA and the rec genes are somehow involved in the repair of spontaneously occurring DNA lesions, since a deficiency in this type of repair may cause lethal sectors. The extent to which spontaneous lethal sectoring (observed in all Rec(-) strains of E. coli studied) may contribute indirectly to the failure to form recombinants is discussed.
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PMID:Spontaneous lethal sectoring, a further feature of Escherichia coli strains deficient in the function of rec and uvr genes. 489 49

Mutants of Escherichia coli K-12 unable to excise pyrimidine dimers from their deoxyribonucleic acid (DNA) because of a uvr mutation show a higher survival when plated on a minimal salts medium after exposure to ultraviolet radiation than when plated on a complex medium such as nutrient agar containing yeast extract. This response has been called minimal medium recovery (MMR). Recovery of uvr mutants can take place in liquid as well as on solid medium, but not in buffer or under conditions of amino acid starvation that do not permit cell growth and normal DNA replication. MMR can thus be distinguished from the recovery of recombination-deficient (rec(-)uvr(+)) derivatives of K-12 which can occur under conditions where growth is not possible. Because MMR is characteristic of excision-defective mutants, it evidently reflects a type of repair independent of excision. We have obtained genetic evidence that MMR is determined by the rec genes, which also control recombination in K-12. Cells carrying a uvr mutation together with recA13, recA56, recB21, or recC22 failed to show MMR and were more sensitive to ultraviolet radiation than either their rec(+)uvr(-) or rec(-)uvr(+) parents. The rec(+)uvr(-) derivatives obtained from recA uvr(-) strains by transduction or by reversion regained the capacity for MMR. Our results indicate that inactivation of any one of the three genes, recA, recB, or recC, prevents cells from showing MMR.
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PMID:Dark-recovery processes in Escherichia coli irradiated with ultraviolet light. 3. Effect of rec mutations on recovery of excision-deficient mutants of Escherichia coli K-12. 491 40

Ultraviolet (UV)-irradiated Escherichia coli K-12 F lac(+) donors transfer damaged F' factors when mated with female cells. Exposure of the zygotes to white light after mating can cause the photoreactivation of the damaged transferred F' factors. In so far as the photoreactivation is specific for pyrimidine dimers, these experiments indicate the presence of UV-induced dimers in the transferred F' factor deoxyribonucleic acid (DNA). These damaged F' factors are remarkably stable in recA recipients, having a half-life for susceptibility to photoreactivation of 1.5 to 2 hr. This is judged by the formation of Lac(+) colonies, all of which are male secondary donors. In crosses with wild type and uvrA, recB, or recC mutant recipients, however, the Lac(+) colonies are predominantly recombinants and photoreactivation is not detected. The extent of DNA synthesis resulting from transfer of F' episomes from irradiated donors suggests that a complementary strand is formed on the damaged template. Photoreactivation behavior and sedimentation properties are used to deduce properties of such damaged episomes. We conclude that the complementary strand is discontinuous directly opposite dimers in the transferred strand. This structure may be an intermediate in the recombinational event sequence in Rec(+) recipients.
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PMID:Properties of F' factor deoxyribonucleic acid transferred from ultraviolet-irradiated donors: photoreactivation in the recipient and the influence of recA, recB, recC, and uvr genes. 492 4


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