Checkpoint mutants (right) are abnormally shaped.
In budding yeast, DNA replication occurs in conjunction with the formation of the bud, which will receive the new set of chromosomes. DNA damage and other stresses activate checkpoint pathways that stall replication forks and start repair. The new papers show that these pathways also stall bud growth to maintain the synchrony between replication and morphology.
Both groups found that mutants of the Rad53 checkpoint kinase continued to elongate their buds during replication stress, when wild-type cells stopped bud growth. Enserink et al. suggest that checkpoint pathways activate a Cdk1-dependent switch, which turns off polar bud growth.
As buds grow, Cdk1 is normally inhibited by Swe1. But checkpoint activation caused Swe1...
