DNA damage response clamp loader Rad24(Rad17) and Mec1(ATR) kinase have distinct functions in regulating meiotic crossovers

Crossover (CO) recombination is essential for chromosome segregation during meiosis I. The number and distribution of COs are tightly regulated during meiosis. CO control includes CO assurance and CO interference, which guarantee at least one CO per a bivalent and evenly-spaced CO distribution, respectively. Previous studies showed the role of DNA damage response (DDR) clamp and its loader in efficient formation of meiotic COs by promoting the recruitment of a pro-CO protein Zip3 and interhomolog recombination, and also by suppressing ectopic recombination. In this study, by classical tetrad analysis of Saccharomyces cerevisiae, we showed that a mutant defective in the RAD24 gene (RAD17 in other organisms), which encodes the DDR clamp loader, displayed reduced CO frequencies on two shorter chromosomes (III and V) but not on a long chromosome (chromosome VII). The residual COs in the rad24 mutant do not show interference. In contrast to the rad24 mutant, mutants defective in the ATR kinase homolog Mec1/Esr1, including a mec1 null and a mec1 kinase-dead mutant, show little or no defect in CO frequency. On the other hand, mec1 COs show defects in interference, similar to the rad24 mutant. Moreover, CO formation and its control are implemented in a chromosome-specific manner, which may reflect a role for chromosome size in regulation.