Morphogenesis and the Cell Cycle

Abstract

Studies of the processes leading to the construction of a bud and its separation from the mother cell in Saccharomyces cerevisiae have provided foundational paradigms for the mechanisms of polarity establishment, cytoskeletal organization, and cytokinesis. Here we review our current understanding of how these morphogenetic events occur and how they are controlled by the cellcycle-regulatory cyclin-CDK system. In addition, defects in morphogenesis provide signals that feed back on the cyclin-CDK system, and we review what is known regarding regulation of cell-cycle progression in response to such defects, primarily acting through the kinase Swe1p. The bidirectional communication between morphogenesis and the cell cycle is crucial for successful proliferation, and its study has illuminated many elegant and often unexpected regulatory mechanisms. Despite considerable progress, however, many of the most puzzling mysteries in this field remain to be resolved.

MSP58 Knockdown Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma in Vitro and in Vivo

“…Cell cycle progression is mainly modulated by two classes of proteins: the cyclins and their kinase partners, the cyclin-dependent kinases (CDKs) (Swanton, 2004;Howell et al, 2012). The G1 to S phase progression is regulated by cyclin-dependent kinase inhibitors (CDKI), such as p21, p27 and p57 (Xiong et al, 1993;Polyak et al, 1994;Matsuoka et al, 1995), and the cyclin D family (Ekholm et al, 2000).…”

Fungal Morphogenesis

“…The obstruction of polarized growth leads to a unicellular lifestyle. Moreover, nuclear division is tightly coordinated with cellular morphogenesis in yeast growth, such that the same cyclindependent protein kinase (CDK) complexes that drive cell-cycle progression also trigger the transitions between polar and nonpolar growth (Wang 2009;Howell and Lew 2012). Furthermore, morphogenetic checkpoints maintain the coordination of nuclear division with polar growth to prevent the formation of anucleate or binucleate cells (Howell and Lew 2012).…”

Budding Yeast Swe1 Is Involved in the Control of Mitotic Spindle Elongation and Is Regulated by Cdc14 Phosphatase during Mitosis

“…Interestingly, a Cdc14 allele defective in its nuclear export was reported to allow mitotic exit but to accumulate a fraction of cells with elongated buds (32). This phenotype could be due to high Swe1 levels or unscheduled Swe1 activity, conditions that interfere with normal isotropic bud growth and cause hyperpolarization of the cells (33). Moreover, Cdc14 and Swe1 were found to physically interact in an high throughput screening (34).…”