Septins Have a Dual Role in Controlling Mitotic Exit in Budding Yeast

In Saccharomyces cerevisiae, the spindle position checkpoint ensures that cells do not exit mitosis until the mitotic spindle moves into the mother/bud neck and thus guarantees that each cell receives one nucleus [1–6]. Mitotic exit is controlled by the small G protein Tem1p. Tem1p and its GTPase ac...

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Bibliographic Details
Published in:	Current biology Vol. 13; no. 8; pp. 654 - 658
Main Authors:	Castillon, Guillaume A., Adames, Neil R., Rosello, Caroline H., Seidel, Hannah S., Longtine, Mark S., Cooper, John A., Heil-Chapdelaine, Richard A.
Format:	Journal Article
Language:	English
Published:	England Elsevier Inc 15-04-2003
Subjects:	Cell Cycle Proteins - metabolism Cytoskeletal Proteins - metabolism Cytoskeletal Proteins - physiology Guanine Nucleotide Exchange Factors - metabolism Microscopy, Fluorescence Mitosis - physiology Monomeric GTP-Binding Proteins - metabolism Mutation - genetics Mutation - physiology Saccharomyces cerevisiae - cytology Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae Proteins - metabolism Spindle Apparatus - physiology
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Summary:	In Saccharomyces cerevisiae, the spindle position checkpoint ensures that cells do not exit mitosis until the mitotic spindle moves into the mother/bud neck and thus guarantees that each cell receives one nucleus [1–6]. Mitotic exit is controlled by the small G protein Tem1p. Tem1p and its GTPase activating protein (GAP) Bub2p/Bfa1p are located on the daughter-bound spindle pole body. The GEF Lte1p is located in the bud. This segregation helps keep Tem1p in its inactive GDP state until the spindle enters the neck. However, the checkpoint functions without Lte1p and apparently senses cytoplasmic microtubules in the mother/bud neck [7–9]. To investigate this mechanism, we examined mutants defective for septins, which compose a ring at the neck [10]. We found that the septin mutants sep7Δ and cdc10Δ are defective in the checkpoint. When movement of the spindle into the neck was delayed, mitotic exit occurred, inappropriately leaving both nuclei in the mother. In sep7Δ and cdc10Δ mutants, Lte1p is mislocalized to the mother. In sep7Δ, but not cdc10Δ, mutants, inappropriate mitotic exit depends on Lte1p. These results suggest that septins serve as a diffusion barrier for Lte1p, and that Cdc10p is needed for the septin ring to serve as a scaffold for a putative microtubule sensor.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0960-9822 1879-0445
DOI:	10.1016/S0960-9822(03)00247-1