Destabilization of the replication fork protection complex disrupts meiotic chromosome segregation

Loss of the FPC protein Swi1 or Swi3 results in reduced spore viability, delayed replication, changes in recombination, reduced centromeric cohesion stability, and chromosome missegregation in meiosis I and II. These phenotypes reveal a crucial link between meiotic replication fork stability and chromosome segregation.
The replication fork protection complex (FPC) coordinates multiple processes that are crucial for unimpeded passage of the replisome through various barriers and difficult to replicate areas of the genome. We examine the function of Swi1 and Swi3, fission yeast’s primary FPC components, to elucidate how replication fork stability contributes to DNA integrity in meiosis. We report that destabilization of the FPC results in reduced spore viability, delayed replication, changes in recombination, and chromosome missegregation in meiosis I and meiosis II. These phenotypes are linked to accumulation and persistence of DNA damage markers in meiosis and to problems with cohesion stability at the centromere. These findings reveal an important connection between meiotic replication fork stability and chromosome segregation, two processes with major implications to human reproductive health.