From 1970s to early 1990s, a lot of cell-cycle regulators such as cell division cycle (cdc) or radiation-sensitive (rad) genes had been identified as results of yeast genetic screenings. In 1988, through the analyses of rad9 mutants in budding yeast (Saccharomyces cerevisiae), Weinert and Hartwell first proposed a cell cycle checkpoint that prevents inappropriate progression of the cell cycle when DNA is damaged or incompletely replicated (Weinert and Hartwell 1988). In 1993, Beach and coworkers reported a novel gene that controls G2/M transition after DNA damage (G2/M checkpoint) in the fission yeast (Schizosaccharomyces pombe). Since this gene encoded a Ser/Thr protein kinase, it was named checkpoint kinase 1 (Chk1) (Walworth et al. 1993). By 1997, Chk1 orthologs were identified in budding yeast (Rad27), fruit fly (Grapes [Grp]; Drosophila melanogaster), mouse, and human (CHEK1indicates a gene locus...
- Reinhardt HC, Hasskamp P, Schmedding I, Morandell S, van Vugt MA, Wang X, et al. DNA damage activates a spatially distinct late cytoplasmic cell-cycle checkpoint network controlled by MK2-mediated RNA stabilization. Mol Cell. 2010;40:34–49. https://doi.org/10.1016/j.molcel.2010.09.018.CrossRefPubMedPubMedCentralGoogle Scholar