DNA double strand break repair in the context of chromatin

In all living organisms, DNA is the basis of genetic information. It is of vital importance to maintain the integrity of this information and to protect it from damage that may arise from intra- or extracellular influences. DNA damage elicits the deployment of an armada of DNA repair factors, consisting of different sets of proteins that can restore an intact DNA molecule in the context of cellular chromatin. Following detection of a DNA lesion, this repair machinery can excise, synthesise, recombine and ligate DNA. Depending on the nature of the damage, it can block cell cycle progression until the damage is repaired, or induce programmed cell death. Hence, the disruption of just one of the repair factors can have deleterious effects. DNA double-strand breaks (DSBs) are one of the most deleterious DNA damages, since when left are unrepaired, they can lead to chromosome fragmentation and loss of genetic information. Yet DSBs are essential for the recombination of genetic material prior to the formation of generative cells, and organisms have developed intricate mechanisms for the various different contexts of DNA repair. In the given collaborative project we aim at elucidating the impact of chromatin environment in the choice of DNA repair pathways and on DNA repair products. We will implement our research plan utilizing innovate and novel molecular tools that are generated in a joint effort. These tools enable us to direct DSB formation to virtually any desired locus in the genome of the model organism of choice (in our case the model plant Arabidopsis thaliana) in either somatic or meiotic cells. We anticipate that the results will be relevant beyond he field of plant biology since the mechanism of DNA repair are conserved.