Checkpoint mutants (right) are abnormally shaped.

DNA damage checkpoint pathways reach out of the nucleus to control cell morphology, according to Smolka et al. (page 743) and Enserink et al. (page 729).

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 degradation and thus Cdk1 activation. Checkpoint mutants, however, were unable to degrade Swe1. They maintained bud-localized growth machinery and a polarized actin network.

Swe1 degradation depends on its localization to septins at the bud neck, where it is phosphorylated. Swe1 localization was normal in checkpoint kinase mutants. Smolka et al. found, however, that Rad53 binds to septins at the bud neck and phosphorylates septins in vitro. Perhaps this modification is a prerequisite to Swe1 phosphorylation.