Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

The iridovirus isolate termed cricket iridovirus (CrIV) was isolated in 1996 from Gryllus campestris L. and Acheta domesticus L. (both Orthoptera, Gryllidae). CrIV DNA shows distinct DNA restriction patterns different from those known for Insect iridescent virus type 6 (IIV-6). This observation led to the assumption that CrIV might be a new species within the family Iridoviridae. CrIV can be transmitted perorally to orthopteran species, resulting in specific, fatal diseases. These species include Gryllus bimaculatus L. and the African migratory locust Locusta migratoria migratorioides (Orthoptera, Acrididae). Analysis of genomic and host range properties of this isolate was carried out in comparison to those known for IIV-6. Host range studies of CrIV and IIV-6 revealed no differences in the peroral susceptibility in all insect species and developmental stages tested to date. Different gene loci of the IIV-6 genome were analyzed, including the major capsid protein (274L), thymidylate synthase (225R), an exonuclease (012L), DNA polymerase (037L), ATPase (075L), DNA ligase (205R) and the open reading frame 339L, which is homologous to the immediate-early protein ICP-46 of frog virus 3. The average identity of the selected viral genes and their gene products was found to be 95.98 and 95.18% at the nucleotide and amino acid level, respectively. These data led to the conclusion that CrIV and IIV-6 are not different species within the Iridoviridae family and that CrIV must be considered to be a variant and/or a novel strain of IIV-6.
J Gen Virol 2002 Feb
PMID:Comparative analysis of the genome and host range characteristics of two insect iridoviruses: Chilo iridescent virus and a cricket iridovirus isolate. 1180 40

Protective immunity to African swine fever virus (ASFV) may involve a combination of both serological and cellular mechanisms. This work is focused on the identification of the possible relevant serological immunodeterminants of immunity. Thus, 14 serological immunodeterminants of ASFV have been characterized by exhaustive screening of a representative lambda phage cDNA expression library of the tissue culture-adapted Ba71V strain of ASFV. The library was constructed using RNA extracted from Vero cells infected for 3, 6, 9 and 12 h. A total of 150 clones was selected arbitrarily by antibody screening of the library with a polyclonal antiserum from a domestic pig surviving infection with the virulent Malta isolate of ASFV. Sequencing of these clones permitted identification of 14 independent viral proteins that stimulated an antibody response. These included six proteins encoded by previously unassigned open reading frames (ORFs) (B602L, C44L, CP312R, E184L, K145R and K205R) as well as some of the more well-studied structural (A104R, p10, p32, p54 and p73) and non-structural proteins (RNA reductase, DNA ligase and thymidine kinase). Immunogenicity of these proteins was confirmed by demonstrating the corresponding antibodies in sera from pigs infected either with the Malta isolate or with the OURT88/3-OURT88/1 isolate combination. Furthermore, the majority of these ORFs were also recognized by immune antiserum from the natural host, the bush pig, following secondary challenge with the virulent Malawi (SINT90/1) isolate of ASFV. Thus, it is possible that some of these determinants may be important in protection against virus infection.
J Gen Virol 2002 Jun
PMID:Identification of the principal serological immunodeterminants of African swine fever virus by screening a virus cDNA library with antibody. 1202 48

Herpesviruses and poxviruses are known to encode the DNA repair enzyme uracil-DNA glycosylase (UNG), an enzyme involved in the base excision repair pathway that specifically removes the RNA base uracil from DNA, while at least one retrovirus (human immunodeficiency virus type 1) packages cellular UNG into virus particles. In these instances, UNG is implicated as being important in virus replication. However, a clear understanding of the role(s) of UNG in virus replication remains elusive. Herpesviruses, poxviruses and some retroviruses encode dUTPase, an enzyme that can minimize the misincorporation of uracil into DNA. The encoding of dUTPase by these viruses also implies their importance in virus replication. An understanding at the molecular level of how these viruses replicate in non-dividing cells should provide clues to the biological relevance of UNG and dUTPase function in virus replication.
J Gen Virol 2002 Oct
PMID:Roles of uracil-DNA glycosylase and dUTPase in virus replication. 1223 14

Increased intracellular concentrations of the initiator protein Rep (or RepA) interfere with pSC101 DNA replication, and mutated Rep proteins that result in an increase in plasmid copy numbers do not inhibit the replication. A rep mutant (rep(inh)) defective in the inhibitory activity was isolated and found to be a new high copy number mutant. The inhibitory function of Rep was enhanced by the coexistence of directly repeated sequences (DR; iterons) in the replication origin region (ori), but not by the inverted repeat sequences (IR) in ori and the rep promoter. This synergistic effect of Rep and DR sequences for the replication inhibition was dependent on their intracellular concentrations. Considering that DR sequences are the specific binding sites of the Rep monomer form, the Rep monomer-DR complex might be responsible for the inhibition of the plasmid replication. Furthermore, the Rep monomer in the crude cell extracts facilitated dimerization of DR DNA fragments by DNA ligase. Neither synergistic inhibitory function with DR nor Rep mediated dimerization of DR DNA was observed in high copy number mutant Rep proteins. The role of the Rep-iteron complex in the copy number control of pSC101 is discussed.
J Gen Appl Microbiol 2000 Feb
PMID:Negative control of plasmid pSC101 replication by increased concentrations of both initiator protein and iterons. 1248 1

We have isolated recombination deficient mutants of Bacillus subtilis on the basis of their sensitivity to methyl-methane-sulfonate or ultraviolet light, or of their inability to be transformed on solid medium. We have analyzed the mutants for several recombination and repair properties; we have grouped them in 5 classes on the basis of their phenotype and tested them for the activity of several enzymes acting on DNA, ie. DNA polymerase, polynucleotide ligase, ATP dependent DNase, and a DNase acting on single-stranded DNA. One mutant was found reduced in the latter DNase. Some of the mutants have been mapped, and they correspond to three different genes denominated rec D, rec F and rec G. All the recombination deficient mutants of B. subtilis described in the literature have been grouped in 7 classes; the mutations belong to 13 (and possibly 15) different genes distributed along the map. A coherent nomenclature and the criteria for a standard study of the rec mutants are proposed.
Mol Gen Genet 1975
PMID:Genetic and enzymic studies on the recombination process in Bacillus subtilis. 1609 63

The protective immune response to African swine fever virus (ASFV) includes both cellular and serological components. In this study, the role of antibodies in the pathogenicity and diagnosis of African swine fever (ASF) was explored. Accordingly, total and Ig isotype antibody responses against the 12 viral proteins previously demonstrated to be the main targets of serological immunity were evaluated in longitudinally collected sera from pigs infected experimentally with the non-pathogenic ASFV/NH/P68 isolate. Strong total IgG antibody responses were observed against viral proteins E183L/p54, K205R/'unassigned', A104R/histone-like and B602L/'unassigned'; therefore, IgM, IgG1 and IgG2 responses to these proteins were also determined. One protein stimulating IgM (K205R) may have practical potential for the detection of recently infected animals. There was a clear trend towards an IgG1 response to all of the proteins. This may reflect a dominant Th2-controlled immune response. In order to identify possible correlations between these serological responses and the pathogenesis of ASF, total IgG responses to the 12 recombinant proteins were compared in asymptomatic and chronically infected animals. For the proteins NP419L/DNA ligase, CP312R, B646L/p73, K196R/thymidine kinase and K205R, the antibody titres were significantly higher in animals developing lesions. One exception was the antibody response to the A104R/histone-like protein, which was higher in asymptomatic than in chronically infected pigs, suggesting that antibodies against this protein might be an indicator of an effective immune response or that this response is somehow involved in protection.
J Gen Virol 2007 Sep
PMID:Systematic analysis of longitudinal serological responses of pigs infected experimentally with African swine fever virus. 1769 51

We previously reported that cells harboring the hepatitis C virus (HCV) RNA replicon as well as those expressing HCV NS3/4A exhibited increased sensitivity to suboptimal doses of apoptotic stimuli to undergo mitochondrion-mediated apoptosis (Y. Nomura-Takigawa, et al., J. Gen. Virol. 87:1935-1945, 2006). Little is known, however, about whether or not HCV infection induces apoptosis of the virus-infected cells. In this study, by using the chimeric J6/JFH1 strain of HCV genotype 2a, we demonstrated that HCV infection induced cell death in Huh7.5 cells. The cell death was associated with activation of caspase 3, nuclear translocation of activated caspase 3, and cleavage of DNA repair enzyme poly(ADP-ribose) polymerase, which is known to be an important substrate for activated caspase 3. These results suggest that HCV-induced cell death is, in fact, apoptosis. Moreover, HCV infection activated Bax, a proapoptotic member of the Bcl-2 family, as revealed by its conformational change and its increased accumulation on mitochondrial membranes. Concomitantly, HCV infection induced disruption of mitochondrial transmembrane potential, followed by mitochondrial swelling and release of cytochrome c from mitochondria. HCV infection also caused oxidative stress via increased production of mitochondrial superoxide. On the other hand, HCV infection did not mediate increased expression of glucose-regulated protein 78 (GRP78) or GRP94, which are known as endoplasmic reticulum (ER) stress-induced proteins; this result suggests that ER stress is not primarily involved in HCV-induced apoptosis in our experimental system. Taken together, our present results suggest that HCV infection induces apoptosis of the host cell through a Bax-triggered, mitochondrion-mediated, caspase 3-dependent pathway(s).
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PMID:Hepatitis C virus infection induces apoptosis through a Bax-triggered, mitochondrion-mediated, caspase 3-dependent pathway. 1876 89

Poxviruses comprise a group of large dsDNA viruses that include members relevant to human and animal health, such as variola virus, monkeypox virus, cowpox virus and vaccinia virus (VACV). Poxviruses are remarkable for their unique replication cycle, which is restricted to the cytoplasm of infected cells. The independence from the host nucleus requires poxviruses to encode most of the enzymes involved in DNA replication, transcription and processing. Here, we use the CRISPR/Cas9 genome engineering system to induce DNA damage to VACV (strain Western Reserve) genomes. We show that targeting CRISPR/Cas9 to essential viral genes limits virus replication efficiently. Although VACV is a strictly cytoplasmic pathogen, we observed extensive viral genome editing at the target site; this is reminiscent of a non-homologous end-joining DNA repair mechanism. This pathway was not dependent on the viral DNA ligase, but critically involved the cellular DNA ligase IV. Our data show that DNA ligase IV can act outside of the nucleus to allow repair of dsDNA breaks in poxvirus genomes. This pathway might contribute to the introduction of mutations within the genome of poxviruses and may thereby promote the evolution of these viruses.
J Gen Virol 2018 06
PMID:Mutagenic repair of double-stranded DNA breaks in vaccinia virus genomes requires cellular DNA ligase IV activity in the cytosol. 2967 20


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