In yeast, cell wall stress originates not only through environmental perturbations but also through normal physiological changes that are coupled to cell cycle progression, as cell wall remodeling and biosynthesis are required to enable the emergence of the growing daughter bud. In S. cerevisiae cell membrane perturbation triggers cell cycle arrest via degradation of Cdc6, a component of the pre-RC53. This is required for cell survival as continued cell cycle progression in the presence of plasma membrane damage induces plasma membrane rupture and cell lysis, leading to cell death53. We found that CDC6 and genes encoding members of the MCM complex that participate in the pre-RC are transcriptionally repressed in response to caspofungin in a Cas5-dependent manner (Fig. 4). To our knowledge, this is the first mechanistic insight into the signaling events that couple cell wall stress with cell cycle arrest in C. albicans, and likely enables the cell to respond to environmental stress without succumbing to cell death. In S. cerevisiae, cell cycle genes are regulated by transcriptional complexes composed of Swi4 and Swi6, including the SBF complex, which is involved in budding and membrane/cell-wall biosynthesis54. We observed that impairment of Cas5 function manifested in more severe misregulation of nuclear division than deletion of SWI4 or SWI6 (Fig. 9), suggesting Cas5 regulates nuclear division largely independent of the SBF complex.