adenosine triphosphate-dependent ligase, ADL, APE1094, ApeLig, ATP-dependent DNA ligase, ATP-dependent DNA ligase 1, ATP-dependent DNA ligase I, ATP-dependent ligase, ATP-dependent ligase LigB, ATP-dependent ligase LigC, ATP-dependent ligase LigD, ATP-type DNA repair ligase, AtuLigD1, AtuLigD2, b-ADL, bacterial ATP-dependent DNA ligase, Cdc9, ChVLig, CVLig, Deoxyribonucleate ligase, Deoxyribonucleic acid joinase, Deoxyribonucleic acid ligase, Deoxyribonucleic acid repair enzyme, Deoxyribonucleic acid-joining enzyme, Deoxyribonucleic joinase, Deoxyribonucleic ligase, Deoxyribonucleic repair enzyme, Deoxyribonucleic-joining enzyme, DNA joinase, DNA ligase, DNA ligase 1, DNA ligase 4, DNA ligase D, DNA ligase I, DNA ligase II, DNA ligase III, DNA ligase IIIalpha, DNA ligase IV, DNA ligase IV homolog, DNA ligase IV-XRCC4 complex, DNA ligase IV/XRCC4 complex, DNA ligase IV/XRCC4/XLF complex, DNA ligase V, DNA ligase VI, DNA repair enzyme, DNA repair ligase D, DNA-joining enzyme, DNAligI, Dnl4, drB0100, Hbu DNA ligase, L3BRCT, LdMNPV DNA ligase, Lig, Lig E, Lig I, Lig III, LIG k alpha, Lig K protein, Lig(Tk), LIG1, Lig3, Lig3alpha, Lig4, LIG6, LigA, ligase 1, ligase D, ligase III, ligase III-alpha, LigB, LigC, LigC1, LigD, LigI, LigIII, LigTh1519, ligTK, MJ0171, MSH-1, Mt-Lig, Mth ligase, MtuLigB, MtuLigC, MtuLigD, NHEJ DNA repair ligase, PabDBD, PaeLigD, PBCV-1 DNA ligase, PF1635, PfLigI, Pfu DNA ligase, PfuLig, Polydeoxyribonucleotide synthase (ATP), Polydeoxyribonucleotide synthase [ATP], Polynucleotide ligase, Sealase, ssLig, SSO0189, T4 ATP ligase, T4 DNA ligase, T4 lig, Vaccinia ligase, Vib-Lig, X4L4, XRCC1/DNA ligase III, XRCC4-DNA ligase IV complex
DNA ligase I deficiency leads to replication-dependent DNA damage and impacts cell morphology without blocking cell cycle progression. LigI deficiency affects the maturation of nascent DNA and increases the frequency of gammaH2AX foci throughout the cell cycle. LigI deficiency leads to chronic activation of the ataxia telangiectasia mutated-mediated DNA damage checkpoint
DNA ligase IV deficiency syndrome (LIG4 syndrome) is a rare autosomal recessive disorder characterized by microcephaly, growth retardation, low birth weight, dysmorphic facial findings, immunodeficiency, pancytopenia, and radiosensitivity due to impaired repair of DNA double-strand breaks by non-homologous end-joining
knockout mutants of lig1 are lethal. lig1-RNAi lines with reduced levels of LIG1 display slower repair of single strand breaks and also double strand breaks
a drB0100 gene deletion mutant exhibits a nearly 2-log cycle reduction in growth rate when exposed to a 10000 Gray dose of gamma-radiation and a significant loss in mitomycin C and methylmethane sulfonate tolerance as compared to the wild type
Arabidopsis atlig6 and lig6/lig4 mutants display significant hypersensitivity to controlled seed ageing, resulting in delayed germination and reduced seed viability relative to wild type lines, and display increased sensitivity to low-temperature stress, resulting in delayed germination and reduced seedling vigour upon transfer to standard growth conditions
deletion of Lig3 results in cellular lethality. Translocations are reduced in frequency in the absence of Lig3. alternative nonhomologous end-joining is impaired with Lig3 loss. Deletion of the zinc finger domain of Lig3, but not the XRCC1-interacting BRCT domain, affects translocation frequency and outcome
inactivation of Lig3 in the mouse nervous system results in mitochondrial DNA loss leading to profound mitochondrial dysfunction, disruption of cellular homeostasis and incapacitating ataxia. Lig3 inactivation causes cardiac failure associated with defective mitochondrial function
DNA ligase III knockdown attenuates the recovery of mtDNA copy number and causes single strand nicks in replicating mtDNA molecules, suggesting the involvement of DNA ligase III in Okazaki fragment ligation in human mitochondria
the level of CTG instability in transgenic DM1 mice with more than 300 CTG repeats which are crossed to mice carrying the homozygous 46BR LigI mutation (only 3% normal activity) and in vitro replication of CTG DNA templates by protein extracts from the 46BR.1G1 LIGI-deficient cell line is assessed. The 46BR LigI enhances CTG contractions in maternal transmissions but not paternal transmissions or somatic tissues. The presence of CTG contractions in oocytes and a replication template-specific effect of the 46BR LigI support a role for LigI in maternal allele-specific CTG instability
human DNA ligase I is considered the main replicative ligase and plays an important role in the joining of Okazaki fragments during lagging strand synthesis
DNA ligase III 3 is a key ligase during base excision repair. DNA ligase III is critical for mitochondrial DNA integrity but not Xrcc1-mediated nuclear DNA repair
LIG6 is required for rapid seed germination and a major determinant of Arabidopsis seed quality and longevity. LIG6 is not essential for the replication of nuclear or organellar genomes. LIG6 has roles in repairing DNA damage accumulated during seed development, storage and/or imbibitions. Lig6 is important for germination vigour under cold temperature stress and for germination under oxidative stress
DNA ligases seal single-strand breaks in double-stranded DNA and their function is essential to maintain the integrity of the genome during various aspects of DNA metabolism, such as replication, excision repair and recombination. DNA-strand breaks are frequently generated as reaction intermediates in these events and the sealing of these breaks depends solely on the proper function of DNA ligase
LigIII functions as the primary ligase in DNA replication in the absence of LigI. A functional redundancy between LigI and LigIII in DNA replication is indicated
using chicken B-cell system DT40 and conditioned knockout strategies it is shown that LIG1 and LIG3 are able to support double-strand break (DSB) repair by backup non-homologous end joining (B-NHEJ) with similar activity in interchangeable manner