Journal
JOURNAL OF CELL SCIENCE
Volume 134, Issue 19, Pages -Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.258972
Keywords
Budding yeast; Mitotic exit network; Spindle pole body
Categories
Funding
- Fondation pour la Recherche Me'ion pour la Recherche Me'dicale (DEQ20150331740 to S.P.), Fondation ARC pour la Recherche sur le Cancer (PJA 20141201926 to S.P.) and Agence Nationale de la Recherche (ANR-18-CE130015-01 to S.P.). [DEQ20150331740]
- Fondation ARC pour la Recherche sur le Cancer [PJA 20141201926]
- Agence Nationale de la Recherche [ANR-18-CE130015-01]
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The activity of the mitotic exit network (MEN) is downregulated by Amn1 protein through a dual mode of action on Tem1 GTPase, inhibiting the reset of the cell cycle clock and leading to rapid extinguishing of MEN activity.
At mitotic exit the cell cycle engine is reset to allow crucial processes, such as cytokinesis and replication origin licensing, to take place before a new cell cycle begins. In budding yeast, the cell cycle clock is reset by a Hippo-like kinase cascade called the mitotic exit network (MEN), whose activation is triggered at spindle pole bodies (SPBs) by the Tem1 GTPase. Yet, MEN activity must be extinguished once MEN-dependent processes have been accomplished. One factor contributing to switching off the MEN is the Amn1 protein, which binds Tem1 and inhibits it through an unknown mechanism. Here, we show that Amn1 downregulates Tem1 through a dual mode of action. On one side, it evicts Tem1 from SPBs and escorts it into the nucleus. On the other, it promotes Tem1 degradation as part of a Skp, Cullin and F-box-containing (SCF) ubiquitin ligase. Tem1 inhibition by Amn1 takes place after cytokinesis in the bud-derived daughter cell, consistent with its asymmetric appearance in the daughter cell versus the mother cell. This dual mechanism of Tem1 inhibition by Amn1 may contribute to the rapid extinguishing of MEN activity once it has fulfilled its functions.
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