The role of homologous recombination in mitotic and meiotic double-strand break repair

All organisms are composed of cells and the cell's nucleus contains DNA. The induction of DNA damage is a threat to organisms. Signalling of DNA damage and subsequent repair is of substantial importance. Double-strand breaks (DSBs) in DNA can be induced by ionising radiation and DNA damaging agents but also arise as intermediates in several cellular processes (e.g. meiosis). DSBs are among the most genotoxic DNA lesions and their accurate repair is crucial. Genetic instability resulting from unrepaired DSBs can lead to cell death and, in a multicellular organism, to cancer. There are two major DSB repair pathways: homologous recombination (HR) and non-homologous endjoining (NHEJ). By NHEJ, broken DNA is sealed together, irrespective of sequence homology, in a not necessarily error-free way. HR, in which a homologous DNA molecule is needed as a template, accurately repairs DSBs. In this thesis we mainly focus on recombinational repair proteins of the RAD52 epistasis group and involved in HR. We analyse the biochemical properties of two Rad52 homologs in S. pombe, Rad22A and Rad22B. We examine combined mutations in RAD52 and RAD54 homologs in S. pombe and mice. We investigate the importance of sumolyation of recombinational repair proteins. We also introduce mice deficient in Sycp1, important for coordination during meiosis and the formation of crossovers