Title

Dma1 prevents mitotic exit and cytokinesis by inhibiting the septation initiation network (SIN)

GSBS Program

Biochemistry & Molecular Pharmacology

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Molecular Genetics and Microbiology

Date

12-14-2002

Document Type

Article

Medical Subject Headings

Cell Cycle Proteins; Cell Division; *Drosophila Proteins; Genes, cdc; Microtubule-Associated Proteins; Microtubules; Mitosis; Mitotic Spindle Apparatus; Models, Biological; Mutation; Protein Structure, Tertiary; Protein-Serine-Threonine Kinases; Schizosaccharomyces; *Schizosaccharomyces pombe Proteins; Signal Transduction

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

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.

Rights and Permissions

Citation: Dev Cell. 2002 Dec;3(6):779-90.

Related Resources

Link to article in PubMed

PubMed ID

12479804