ArticleMolecular biology of the cell2020
Spindle pole bodies function as signal amplifiers in the Mitotic Exit Network.
Article in Molecular biology of the cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- A noncanonical GTPase signaling mechanism controls exit from mitosis in budding yeast.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cell growth and nutrient availability control the mitotic exit signaling network in budding yeast.The Journal of cell biology · 2024Article
- A noncanonical GTPase signaling mechanism controls exit from mitosis in budding yeast.bioRxiv : the preprint server for biology · 2024Article
- The signalling lipid PI3,5POpen biology · 2023Article
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- Unifying the mechanism of mitotic exit control in a spatiotemporal logical model.PLoS biology · 2020Article
- Sas4 links basal bodies to cell division via Hippo signaling.The Journal of cell biology · 2020Article
- Sperm centriole assessment identifies male factor infertility in couples with unexplained infertility - a pilot study.European journal of cell biologyArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Mitotic Exit Network (MEN), a budding yeast Ras-like signal transduction cascade, translates nuclear position into a signal to exit from mitosis. Here we describe how scaffolding the MEN onto spindle pole bodies (SPB-centrosome equivalent) allows the MEN to couple the final stages of mitosis to spindle position. Through the quantitative analysis of the localization of MEN components, we determined the relative importance of MEN signaling from the SPB that is delivered into the daughter cell (dSPB) during anaphase and the SPB that remains in the mother cell. Movement of half of the nucleus into the bud during anaphase causes the active form of the MEN GTPase Tem1 to accumulate at the dSPB. In response to Tem1's activity at the dSPB, the MEN kinase cascade, which functions downstream of Tem1, accumulates at both SPBs. This localization to both SPBs serves an important role in promoting efficient exit from mitosis. Cells that harbor only one SPB delay exit from mitosis. We propose that MEN signaling is initiated by Tem1 at the dSPB and that association of the downstream MEN kinases with both SPBs serves to amplify MEN signaling, enabling the timely exit from mitosis.
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Registered trials
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