Arabidopsis DNA ligase IV is induced by γ-irradiation and interacts with an Arabidopsis homologue of the double strand break repair protein XRCC4
Article first published online: 25 DEC 2001
The Plant Journal
Volume 24, Issue 1, pages 67–78, October 2000
How to Cite
West, C. E., Waterworth, W. M., Jiang, Q. and Bray, C. M. (2000), Arabidopsis DNA ligase IV is induced by γ-irradiation and interacts with an Arabidopsis homologue of the double strand break repair protein XRCC4. The Plant Journal, 24: 67–78. doi: 10.1046/j.1365-313x.2000.00856.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- Received 24 February 2000; revised 22 June 2000; accepted 12 July 2000.
- DNA repair;
- non-homologous end joining;
- BRCT domain
Rejoining of single- and double-strand breaks (DSBs) introduced in DNA during replication, recombination, and DNA damage is catalysed by DNA ligase enzymes. Eukaryotes possess multiple DNA ligase enzymes, each having distinct roles in cellular metabolism. Double-strand breaks in DNA, which can occur spontaneously in the cell or be induced experimentally by γ-irradiation, represent one of the most serious threats to genomic integrity. Non-homologous end joining (NHEJ) rather than homologous recombination is the major pathway for repair of DSBs in organisms with complex genomes, including humans and plants. DNA ligase IV in Saccharomyces cerevisiae and humans catalyses the final step in the NHEJ pathway of DSB repair. In this study we identify an Arabidopsis thaliana homologue (AtLIG4) of human and S. cerevisiae DNA ligase IV which is shown to encode an ATP-dependent DNA ligase with a theoretical molecular mass of 138 kDa and 48% similarity in amino-acid sequence to the human DNA ligase IV. Yeast two-hybrid analysis demonstrated a strong interaction between A. thaliana DNA ligase IV and the A. thaliana homologue of the human DNA ligase IV-binding protein XRCC4. This interaction is shown to be mediated via the tandem BRCA C-terminal domains of A. thaliana DNA ligase IV protein. Expression of AtLIG4 is induced by γ-irradiation but not by UVB irradiation, consistent with an in vivo role for the A. thaliana DNA ligase IV in DSB repair.