EC Number   |
General Information |
Reference |
|---|
   6.5.1.1 | malfunction |
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 |
714069 |
| 6.5.1.1 | malfunction |
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 |
716537 |
| 6.5.1.1 | malfunction |
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 |
716669 |
| 6.5.1.1 | malfunction |
disruption of MSH-1 results directly in resistance to monensin, salinomycin, and methylnitrourea |
713775 |
| 6.5.1.1 | malfunction |
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 |
709931 |
| 6.5.1.1 | malfunction |
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 |
714345 |
| 6.5.1.1 | malfunction |
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 |
710211 |
| 6.5.1.1 | malfunction |
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 |
716334 |
| 6.5.1.1 | malfunction |
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 |
707895 |
| 6.5.1.1 | malfunction |
Lig1-deficient 46BR.1G1 cells are hypomutable by DNA damage |
709055 |
