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:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fusions of the lac operon to genes induced by treatment with sublethal levels of alkylating agents have been selected from random insertions of the Mu-dl(ApRlac) phage by screening for induction of beta-galactosidase activity in the presence of methyl methanesulfonate. Genetic analysis reveals that these fusions resulted from insertion of Mu-dl(ApRlac) into two regions of the chromosome. One region (aidA) is near his and, based on phenotypic effects, appears to represent insertion into the alkA gene. The other region (aidB) is in the 92.3- to 98-min region, which harbors no previously identified genes involved in repair of alkylation damage. The aidB fusions caused increased resistance to alkylating agents and caused little or no change in the biological effects of adaptation to alkylating agents. Unlike the aidA fusions, aidB fusions showed increased beta-galactosidase activity in untreated cells in a growth phase-dependent fashion. The ada-5 mutation, which blocks expression of the adaptive response, decreased induction of beta-galactosidase activity in both aidA and aidB fusions after alkylation treatments. Thus, both aidA and aidB share with adaptive response a common regulatory mechanism involving the ada gene. The growth phase-dependent control of the aidB fusions, however, is unaffected by ada, suggesting that a second regulatory mechanism exists that controls only aidB.
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PMID:Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents. 633 Jul 40

The product of the uvrD gene of Escherichia coli is involved in the repair of DNA damage, mismatch repair, and recombination. Phage Mud(Amp, Lac) was used to form a uvrD-lacZ fusion allowing uvrD expression to be followed by measuring the activity of beta-galactosidase, the product of the lacZ gene. uvrD expression was inducible by DNA damage and was under the control of lexA-recA regulatory system. Mutations in the uvrD gene that result in different phenotypes in respect to DNA repair and spontaneous mutation have been previously found. The phenotype of the uvrD::Mud(Amp, Lac) mutant was mutator and UV-sensitive but not as deficient in host cell reactivation or repair of methyl methanesulfonate damage as the previously described uvrD3 mutant.
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PMID:The Escherichia coli uvrD gene is inducible by DNA damage. 635 63

A new mutation in Escherichia coli K12, isfA, is described, which causes inhibition of SOS functions. The mutation, discovered in a delta polA+ mutant, is responsible for inhibition of several phenomena related to the SOS response in polA+ strains: UV- and methyl methanesulfonate-induced mutagenesis, resumption of DNA replication in UV-irradiated cells, cell filamentation, prophage induction and increase in UV sensitivity. The isfA mutation also significantly reduces UV-induced expression of beta-galactosidase from recA::lacZ and umuC'::lacZ fusions. The results suggest that the isfA gene product may affect RecA* coprotease activity and may be involved in the regulation of the termination of the SOS response after completion of DNA repair. The isfA mutation was localized at 85 min on the E. coli chromosome, and preliminary experiments suggest that it may be dominant to the wild-type allele.
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PMID:A new mutation in Escherichia coli K12, isfA, which is responsible for inhibition of SOS functions. 765 21

A 4.3-kb EcoRI fragment from a Lactococcus lactis genomic library alleviates the methyl methanesulfonate, mitomycin C, and UV sensitivities of an Escherichia coli recA mutant (M. Novel, X. F. Huang, and G. Novel, FEMS Microbiol. Lett. 72:309-314, 1990). It complements recA1 and delta recA mutations but not recA13. Three proteins (with molecular masses of 20, 35, and 23 kDa) were produced from this fragment in a T7-directed system, and three corresponding genes were detected by DNA sequencing, namely, ISS1CH;lacX, which is the distal gene of the lac operon; and a third open reading frame, named lacN, which encodes 211 amino acids. Mutations produced in either lacX or in lacN resulted in the loss of the resistance to DNA-damaging agents. Thus, these two genes appeared to be involved in this activity. Introduction of pUCB214 carrying the 4.3-kb fragment into a lexA+ delta recA306 sfiA::lacZ strain resulted in UV-inducible synthesis of beta-galactosidase. A uvrA strain or a lexA (Ind-) strain containing pUCB214 did not support any DNA repair. However, a lexA (Def-) strain carrying pUCB214 could partly repair UV damage. We discuss possible targets for LacX and LacN products, and we speculate that LacX and LacN may constitute a two-component regulatory system that is able to respond to SOS signals, and then to act in the SOS response, bypassing the RecA-activated function.
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PMID:Two Lactococcus lactis genes, including lacX, cooperate to trigger an SOS response in a recA-negative background. 781 16

Methyl methanesulfonate (MMS) is an extraordinarily poor mutagen compared to ethylnitrosourea (ENU) or even X-rays. In lung fibroblasts in vivo, MMS has been shown to induce many micronuclei but few, if any, mutations at the hpt locus. We wondered if the lack of mutations might be due to the lack of division and DNA synthesis in fibroblasts in vivo, which would permit substantial time for differential repair of DNA lesions. This idea was tested in the small intestine, a tissue in which the cells are actively dividing. Two loci were examined: a native locus (Dlb-1) which determines the presence or absence of a lectin binding site on the surface of the epithelial cells, and a lacl transgene which controls beta-galactosidase synthesis. Locl mutations were detected after in vitro packaging of DNA isolated from the intestinal epithelium into lambda phage and expression in suitable bacteria. Although the epithelial cells are proliferating, acute treatments produced no significant increase in mutations at either locus. Subacute treatments produced low but significant increases in mutation frequency at both loci. The results confirm that MMS is a far more potent clastogen than it is a mutagen and should be regarded as a super-clastogen in the same manner as ENU is a super-mutagen. The carcinogenicity of MMS is probably the result of its potent clastogenicity rather than its weak activity as a point mutagen.
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PMID:Mutagenicity of methyl methanesulfonate (MMS) in vivo at the Dlb-1 native locus and a lacI transgene. 822 13

In order to study mitotic homologous recombination in somatic Drosophila melanogaster cells in vitro and to learn more on the question how recombination is influenced by mutagens, a genetic system was developed where spontaneous and drug-induced recombination could be monitored. Two recombination reporter substrates were stably introduced in multiple copies into the genome of established D. melanogaster Schneider line 2 cells: one plasmid (pSB310) contained the 5' and 3' deleted neomycin phosphoribosyltransferase alleles neoL and neoR as direct repeats; the other (pSB485) contained similar deletions (lacZL and lacZR) of the beta-galactosidase gene (lacZ). Restoration of a functional neo gene upon mitotic recombination between homologous sequences allowed direct selection for the event, whereas recombination in single cells harbouring the integrated lacZ-based reporter plasmid was detected by histochemical staining or flow cytometric analysis (FACS). The neo-based construct in the clonal transgenic cell line 44CD4 showed a spontaneous recombination frequency of 2.9 x 10(-4), whereas the 485AD1 cell line harbouring the lacZ-based construct exhibited a frequency of 2.8 x 10(-4). The alkylating agents EMS and MMS and the clastogen mitomycin C were able to induce recombination in the 485AD1 cell line in a dose-dependent manner. The results obtained from these studies suggest that the transgenic cell lines are potentially useful tools for identifying agents which stimulate direct repeat recombination in somatic Drosophila cells.
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PMID:A genetic system to detect mitotic recombination between repeated chromosomal sequences in Drosophila Schneider line 2 cells. 946 10

Vascular senescence is closely associated with age-related vascular disorders and is enhanced by angiotensin (Ang) II type 1 receptor stimulation. However, the role of Ang II type 2 receptor activation in vascular senescence is still an enigma. Ang II stimulation significantly increased senescence-associated beta-galactosidase activity and the level of 8-hydroxy-2'-deoxyguanosine, with enhancement of oxidative stress and expression of Ki-ras2A, p53, and p21 in vascular smooth muscle cells (VSMCs) from wild-type (Agtr2(+)) mice, whereas these effects of Ang II were enhanced in VSMCs from Ang II type 2 receptor null (Agtr2(-)) mice. Administration of an Ang II type 1 receptor blocker, valsartan, attenuated these parameters, with less effect in Agtr2(-) VSMCs. Ang II stimulation increased methyl methanesulfonate sensitive 2 (MMS2) expression in Agtr2(+) VSMCs but not in Agtr2(-) VSMCs. MMS2 small-interfering RNA treatment enhanced Ang II-induced senescence-associated beta-galactosidase activity and 8-hydroxy-2'-deoxyguanosine level with no significant changes in oxidative stress markers and the expression of Ki-ras2A, p53, and p21. Moreover, exposure of Agtr2(+) VSMCs to hydrogen peroxide and ultraviolet irradiation induced marked increases in senescence-associated beta-galactosidase activity and 8-hydroxy-2'-deoxyguanosine level, which were further enhanced in Agtr2(-) and MMS2 small-interfering RNA-treated Agtr2(+) VSMCs. Agtr2(+) mice exposed to x-ray irradiation showed increases in senescence-associated beta-galactosidase activity and 8-hydroxy-2'-deoxyguanosine level in the aorta, which were further exaggerated in the aorta of Agtr2(-) mice with a lower MMS2 level. These findings suggest that Ang II type 2 receptor signaling attenuates DNA damage and consequent vascular senescence at least in part through MMS2 transactivation and propose the beneficial effects of Ang II type 2 receptor stimulation with Ang II type 1 receptor blockers in age-related vascular disorders.
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PMID:Angiotensin II type 2 receptor deletion enhances vascular senescence by methyl methanesulfonate sensitive 2 inhibition. 1836 23


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