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Query: EC:6.5.1.2 (DNA ligase)
 2,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sensitive and quantitative assay for DNA ligase has been developed which is suitable for the analysis of crude cell extracts of yeast. The assay is sufficiently sensitive to detect the low levels of DNA ligase activity remaining in cdc9 mutants of Saccharomyces cerevisiae. Indeed, we have been able to show that this residual activity is temperature-sensitive, thus establishing finally that CDC9 is the structural gene for DNA ligase.
Mol Gen Genet 1985
PMID:An improved assay for DNA ligase reveals temperature-sensitive activity in cdc9 mutants of Saccharomyces cerevisiae. 390 Jun 39

When Escherichia coli carrying a thermosensitive mutation in DNA ligase was grown at the restrictive temperature, several functions associated with the SOS system were induced. These included lambda prophage induction, W-reactivation and W-mutagenesis of ultraviolet-irradiated lambda phage, and recA protein synthesis, all of which were lexA+ recA+ recB+ dependent and chloramphenicol sensitive, and lexA+-dependent filamentation. These results indicate that ligase-deficient growth leads to the induction of the SOS system, and that all the above functions may respond to common induction signals.
J Gen Microbiol 1982 Mar
PMID:Induction of the SOS system by DNA ligase-deficient growth of Escherichia coli. 621 Jul 61

We have constructed a hybrid plasmid molecule that contains the complete coding sequences from the 26S mRNA of Semliki Forest virus. Five fragments which together covered the mRNA sequence were isolated from three original hybrid plasmids and joined together at five different restriction endonuclease cleavage sites using T4 DNA ligase.
J Gen Virol 1982 Feb
PMID:Construction of a hybrid plasmid molecule containing the total coding region of Semliki Forest virus 26S mRNA. 627 65

The drug hydroxyurea has been found to affect the conditional DNA ligase mutant cdc9 in the same way as a wild type. Specific concentrations inhibit the joining of completed replicons leading to a substantial accumulation of these molecules. Upon removal of hydroxyurea and further incubation of cdc9 cells at the permissive temperature the replicons joined together, while in sharp contrast at the restrictive temperature no such joining occurred. However, a revertant of cdc9 able to grow at the restrictive temperature was also able to join replicons under these conditions, so the cdc9 ligase must be responsible for the assembly of completed replicons.
Mol Gen Genet 1983
PMID:The cdc9 ligase joins completed replicons in baker's yeast. 634 75

Monomeric pBR322 DNA that had been linearized at its unique SalI site transformed wild-type Escherichia coli with 10(2) to 10(3) times less efficiency than CCC plasmid DNA. Dose-response experiments indicated that a single linear plasmid 'molecule' was sufficient to produce a transformant. Transformation with linearized pBR322 DNA was reduced 10 to 40 fold in recA1 , recBC- or recF- backgrounds. In contrast, transformation with CCC DNA was unaffected by the rec status of the host. Transformation with linear pBR322 DNA was increased 3-fold in a DNA ligase-overproducing ( lop11 ) mutant and decreased to a similar degree by transient inactivation of ligase in a ligts7 mutant. A proportion (ranging from about 9% in the wild-type to 42% in a recBC, lop11 mutant) of the transformants obtained with SalI-linearized pBR322 monomeric DNA contained deleted plasmids. Deletion rates were generally higher in rec- strains. Dephosphorylation of the termini on linear DNA or the creation of blunt-ended pBR322 molecules (by end-filling the SalI 5' protrusions or by cleavage with PvuII) decreased the transformation frequency whilst increasing the deletion rate. Linear pBR322 dimeric DNA gave transformation frequencies in recA+ and recA- strains that were reduced only 3 to 7 fold respectively relative to frequencies obtained with dimeric CCC DNA. Furthermore, in contrast to transformation with linear monomeric DNA, deletions were not observed. We propose that the majority of transformants arise, not by simple intracellular reannealing and ligation of the two cohesive SalI-termini of a linear molecule, but by intramolecular recombination.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Gen Genet 1984
PMID:Recombination-dependent recircularization of linearized pBR322 plasmid DNA following transformation of Escherichia coli. 637 76

Fanconi's anemia, a hereditary autosomal disease with chromosomal instability, elevated incidence of cancer and clinical symptoms is accompanied by a DNA repair deficiency. Fibroblasts from patients with Fanconi's anemia were found to be impaired in the DNA repair of UV damage. Nucleoid decondensation and recondensation after UV irradiation were less efficient in fibroblasts from patients with Fanconi's anemia than in those from a healthy proband. These data confirm our earlier findings that DNA ligase is deficient in Fanconi's anemia.
Mol Gen Genet 1982
PMID:UV-repair is impaired in fibroblasts from patients with Fanconi's anemia. 695 46

The nucleotide sequence of a 55098 bp region from the right end of the genome of a virulent African swine fever virus (ASFV) isolate (Malawi LIL20/1) has been determined. Translation of the sequence identified 67 major open reading frames (ORFs) which are closely spaced and read from both DNA strands. At six positions intergenic tandem repeat arrays are found. Comparison of the predicted amino acid sequences of encoded proteins with protein sequence databases identified a number of homologies. These include three subunits of RNA polymerase, a protein with homology to transcription factor SII (TFSII), a DNA ligase, two subunits of mRNA capping enzyme, a DNA topoisomerase type II, a dUTPase, a protein kinase, three helicases, a ubiquitin-conjugating enzyme, a protein with homology to the nif S and nif S-like proteins identified in some bacteria and Saccharomyces cerevisiae, a protein with homology to both a myeloid differentiation primary response antigen (MyD116) and to a herpes simplex virus-encoded neurovirulence-associated protein (ICP34.5), a protein with homology to the ASFV-encoded structural protein p22, two proteins with homology to copies of the ASFV-encoded multigene family 360 and one protein with homology to the ASFV-encoded multigene family 110. Four genes encode proteins which have homology to each other and constitute a new multigene family (MGF100). Nine ORFs encode proteins which contain predicted transmembrane domains. The possible functions of these predicted ASFV-encoded proteins are discussed and the evolutionary relationship of ASFV to other viruses are considered. Despite the similarities in genome structure and replication strategy of ASFV with poxviruses, sequence similarity between them is low and the organization of ASFV-encoded genes is not colinear with that of the orthopoxviruses.
J Gen Virol 1994 Jul
PMID:Nucleotide sequence of a 55 kbp region from the right end of the genome of a pathogenic African swine fever virus isolate (Malawi LIL20/1). 802 96

Uracil-DNA glycosylase encoded in many species functions as a DNA repair enzyme that removes uracil residues from DNA. To investigate the potential function of uracil-DNA glycosylase encoded by human herpes-virus 6 (HHV-6), we sequenced a DNA clone (pSTY09), identified an open reading frame of 765 bp and compared the putative amino acid sequence with other uracil-DNA glycosylases, by computer analysis. The amino acid sequence of HHV-6 had similarities to other uracil-DNA glycosylases, with the highest degree of similarity to those of human cytomegalovirus and Epstein-Barr virus. Two strongly conserved regions in uracil-DNA glycosylase of other species also existed in HHV-6. The gene product which was expressed in Escherichia coli demonstrated uracil-DNA glycosylase activity. This is the first report to identify and characterize the uracil-DNA glycosylase gene in HHV-6.
J Gen Virol 1994 Sep
PMID:Identification of human herpesvirus 6 uracil-DNA glycosylase gene. 807 33

A fragment of 4156 bp of fowlpox virus (FPV) genomic DNA contains homologues of vaccinia virus 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase (3 beta-HSD; A44L) and DNA ligase (A50R) genes. The FPV locus has clearly been rearranged relative to that of vaccinia virus as homologues of genes A45R to A49R, including the thymidylate kinase and a gene with homology to superoxide dismutase, are deleted. The deleted genes are replaced by two open reading frames: for a serine proteinase inhibitor with homology to vaccinia virus gene K2L and for a protein with no significant homology to proteins in the databases. In addition, the FPV homologues of A44L and A50R are in the same polarity in FPV whereas they are in opposite polarities in vaccinia virus. Increased 3 beta-HSD activity has been demonstrated in cells infected with either of two different strains of FPV or with canarypox virus.
J Gen Virol 1994 Sep
PMID:Deletion of fowlpox virus homologues of vaccinia virus genes between the 3 beta-hydroxysteroid dehydrogenase (A44L) and DNA ligase (A50R) genes. 807 53

The mutations spectra of cis-syn, trans-syn-I, (6-4), and Dewar pyrimidone photoproducts of the TT site of AATTAA and TATTAT in the (-) strand of a heteroduplex M13 vector were obtained in an excision and photoreversal repair deficient Escherichia coli host under SOS conditions. Oligonucleotides containing site-specific photoproducts were annealed to a complementary uracil-containing (+) strand that contained one or more unique pairs of nucleotide mismatches and used to prime (-) strand synthesis with a DNA polymerase and dNTPs. Following DNA synthesis, the reaction mixtures were incubated with T4 DNA ligase and ATP and then used to transfect SOS-induced competent CSRO6F' cells (uvrA6 and phr-1). The transfectants were plated, gridded, and probed by oligonucleotides specific for progeny of the (-) and (+) strands. Individual progeny of the photoproduct-containing (-) strands were plaque purified and sequenced by the dideoxy method. The cis-syn and trans-syn-I dimers were found not to be very mutagenic (<9%), the Dewar product more so (<33%), and the (6-4) product the most mutagenic (<73%). The mutation spectra were similar to those previously reported for the same photoproducts of the TT site of AGTTGG in the (+) strand of an M13 vector [Lawrence, C. W., et al. (1990) Mol. Gen Genet. 222, 166-168; LeClerc, J. E., et al. (1991) Proc. Natl. Acad. Sci. U.S.A. 88, 9685-9689] except that -1 deletion mutations were not observed for the trans-syn-I photoproducts, and a lower frequency of 3'-T-->C mutations was observed for the (6-4) photoproduct. Evidence that a small percentage of (+) strand repair of a double mismatch to the 3'-side of the photoproduct. Evidence that a small percentage of (+) strand repair of a double mismatch to the 3'-side was obtained from transfection experiments in which a second double mismatch was introduced opposite or flanking the photoproduct. Analysis of the minor tandem mutations induced by the (6-4) and Dewar products suggests that the SOS polymerase complex is able to elongate what amounts to double mismatches opposite these photoproducts and is consistent with the action of a highly processive polymerase that lacks proofreading ability.
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PMID:Mutation spectra of M13 vectors containing site-specific Cis-Syn, Trans-Syn-I, (6-4), and Dewar pyrimidone photoproducts of thymidylyl-(3'-->5')-thymidine in Escherichia coli under SOS conditions. 867 50


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