The role of DNA damage kinase DDK in meiotic recombination

Meiosis is a specialized cell division program, which is essential for the generation of haploid germ cells. Reduction of the chromosome content in meiosis is necessary to compensate for the doubling of chromosome numbers after fertilization. Meiosis also contributes to genetic diversity by reciprocal exchanges of paternal and maternal chromosome portions. Defects in meiotic cell divisions are the leading cause of miscarriages and diseases linked to mental retardation. During prophase of the first meiotic division a tether is made between the parental homologous chromosomes, which aids their faithful segregation. This is achieved by the pairwise alignment of the parental homologs, the induction of DNA double-strand breaks, their repair via mechanisms that allow this physical tether to be formed, and the installation of the synaptonemal complex. These processes are tightly regulated to orchestrate chromosome morphogenesis, DNA double strand break repair and cell cycle progression. Additionally, DNA repair in meiosis can follow alternative paths which often serve as backup programs. However, how these paths are suppressed in the wild type and how the predominant repair pathways are reinforced is not fully understood. Dbf4-dependent kinase (DDK) plays a major role in regulating multiple important steps in yeast meiosis; it remains to be understood whether it is equally important for meiosis in animals. We want to use the simple animal model system Caenorhabditis elegans to generate a framework whether and how Dbf4-dependent kinase (DDK) contributes to successful meiosis in animals by employing a combination of cell biological, biochemical and genetic methods.