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DNA Ligases I and III Support Nucleotide Excision Repair in DT 40 Cells with Similar Efficiency
Author(s) -
PaulKonietzko Katja,
Thomale Juergen,
Arakawa Hiroshi,
Iliakis George
Publication year - 2015
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12487
Subject(s) - nucleotide excision repair , dna repair , pyrimidine dimer , biology , dna ligase , microbiology and biotechnology , dna , genetics
In eukaryotic cells helix‐distorting DNA lesions like cyclobutane pyrimidine dimers ( CPD s) and 6–4 pyrimidine‐pyrimidone photoproducts (6–4 PP s) are efficiently removed by nucleotide excision repair ( NER ). NER is a multistep process where in the end, subsequent to replication over the gap, the remaining nick is sealed by a DNA ligase. Lig1 has been implicated as the major DNA ligase in NER . Recently, Lig3 has been implicated as a component of a NER subpathway that operates in dividing cells, but which becomes particularly important in nondividing cells. Here, we use DT 40 cells and powerful gene targeting approaches for generating DNA ligase mutants to examine the involvement and contribution of Lig1 and Lig3 in NER using cell survival measured by colony formation, and repair kinetics of CPD by immunofluorescence microscopy and immuno‐slot‐blotting. Our results demonstrate an impressive and previously undocumented potential of Lig3 to substitute for Lig1 in removing helix‐distorting DNA lesions by NER in proliferating cells. We show for the first time in a clean genetic background a functional redundancy in NER between Lig1 and Lig3, which appears to be cell cycle independent and which is likely to contribute to the stability of vertebrate genomes.