The S-phase checkpoint has roles in all phases of the cell cycle, which has implications for the majority of cancers that lack cell cycle controls.

The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

Daughter-cell-associated factors and centrosome-based regulation is important in mitotic exit and spindle position checkpoint control.

Cdc7 and CK1g1 independently and additively phosphorylate the Chk1-binding domain of claspin to activate replication checkpoint with differential contribution of each kinase in different cell types.

The mechanism behind the recruitment of the spindle assembly checkpoint protein BubR1 to the kinetochore illustrates how gene duplication and sub-functionalization can influence the functional complexity of a protein network.

During meiosis, budding yeast use a checkpoint involving the protein Mec1 to prevent the formation of double-strand breaks in DNA that has not completed replication.

Activation of a DNA-damage cell cycle checkpoint during aging causes genome instability and senescence in yeast mother cells.

The spindle assembly protein Bub3 recruits the checkpoint kinase Bub1 to kinetochores by binding to phosphorylated MELT repeats in the kinetochore subunit Knl1.

Cell biological and genetic analyses reveal how budding yeast cells optimize Spindle Assembly checkpoint signaling to maximize chromosome segregation accuracy and minimize unnecessary delays in anaphase onset.

Chromosomal instability through spindle assembly checkpoint alleviation facilitates malignant transformation of hepatocytes and T-cells in vivo, resulting in cancers with recurrent karyotypes.