Abstract
Double-strand DNA breaks (DSBs) are the most threatening type of DNA damages in living cells. For the maintenance of genome integrity and cell survival, it is critical that cells repair such breaks accurately and faithfully. Cells possess two major repair pathways, homologous recombination (HR) and non-homologous end joining (NHEJ), to deal with DSBs. The completion of genome sequencing of Arabidopsis<I/> and several major crops has greatly facilitated the search and study of genes involved in HR and NHEJ. A number of homologous genes involved in DSB repair in yeast and vertebrates have been identified in higher plants. The recent studies with Arabidopsis<I/> mutants deficient in DSBs repair have been showing many similarities and several important differences of the mechanisms between higher plants and vertebrates. For example, these DSBs repair-deficient mutants clearly showed hypersensitivity to DSBs-inducing agents, but did not show embryonic lethality or severe growth defects, which is in contrast to cases in vertebrate animals. This may represent a distinct advantage of plant systems for the study of DSBs repair and mutations arising during the repair.
In this presentation, the current understanding of DSB repair and its role in mutagenesis in higher plants will be discussed. Especially, we would like to discuss about the analysis of mutations created by DSBs introduced with zinc finger nucleases, and its mutations in DSBs repair deficient mutant plants.
