Dma1 prevents mitotic exit and cytokinesis by inhibiting the septation initiation network (SIN)
Biochemistry & Molecular Pharmacology
Graduate School of Biomedical Sciences; Department of Molecular Genetics and Microbiology
Life Sciences | Medicine and Health Sciences
In the fission yeast Schizosaccharomyces pombe, the septation initiation network (SIN) triggers cytokinesis after mitosis. We investigated the relationship between Dma1p, a spindle checkpoint protein and cytokinesis inhibitor, and the SIN. Deletion of dma1 inactivates the spindle checkpoint and allows precocious SIN activation, while overexpressing Dma1p reduces SIN signaling. Dma1p seems to function by inhibiting the SIN activator, Plo1p kinase, since dma1 overexpression and deletion phenotypes suggest that Dma1p antagonizes Plo1p localization. Furthermore, failure to maintain high cyclin-dependent kinase (CDK) activity during spindle checkpoint activation in dma1 deletion cells requires Plo1p. Dma1p itself localizes to spindle pole bodies through interaction with Sid4p. Our observations suggest that Dma1p functions to prevent mitotic exit and cytokinesis during spindle checkpoint arrest by inhibiting SIN signaling.
DOI of Published Version
Dev Cell. 2002 Dec;3(6):779-90.
Guertin DA, Venkatram S, Gould KL, McCollum D. (2002). Dma1 prevents mitotic exit and cytokinesis by inhibiting the septation initiation network (SIN). GSBS Student Publications. https://doi.org/10.1016/S1534-5807(02)00367-2. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/451