ASYMMETRY IN MEN

Generation of asymmetry in mitotic exit network (MEN) signaling

Coordinatore	UNIVERSIDAD DE SEVILLA    more  Organization address address: CALLE S. FERNANDO 4 city: SEVILLA postcode: 41004 contact info Titolo: Ms. Nome: Margarita Cognome: Martínez-Pais Loscertales Email: send email Telefono: +34 954 48 81 29 Fax: -954488083
Nazionalità Coordinatore	Spain [ES]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-IRG-2008
Funding Scheme	MC-IRG
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-01-01   -   2013-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSIDAD DE SEVILLA  Organization address address: CALLE S. FERNANDO 4 city: SEVILLA postcode: 41004 contact info Titolo: Ms. Nome: Margarita Cognome: Martínez-Pais Loscertales Email: send email Telefono: +34 954 48 81 29 Fax: -954488083	ES (SEVILLA)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'The mitotic exit network (MEN) is a signaling pathway that promotes exit from mitosis in Saccharomyces cerevisiae by maintaining the protein phosphatase Cdc14 released from the nucleolus into the nucleus and the cytoplasm, where it eventually promotes mitotic cyclin degradation. MEN resembles a RAS-like signaling cascade. The GTPase Tem1 and the two component GTPase-activating protein Bfa1-Bub2, which function at the top of the MEN, have been shown to localize only to the spindle pole body (SPB, the yeast’s centrosome) that enters the daughter cell during anaphase, while they are excluded from the SPB that stays in the mother cell. Based on our observations, the differential localization of Bfa1, Bub2, and Tem1 to SPBs is determined by a different efficiency in loading of the complex onto the SPBs that is dependent on specific microtubule-cortex interactions. We have also found that polarization of the actin cytoskeleton plays an important role in the generation of the asymmetry. However, the determinants of this asymmetry and the exact mechanism are still unknown. The objectives of this proposal are to: (i) Evaluate the role played on this asymmetry by proteins that either interact with the Tem1 complex or involved in other processes of generation of polarity; (ii) Perform genetic screens to identify genes required for the asymmetric localization of Bfa1, Bub2 and Tem1; (iii) Identify the regions within Bfa1, Bub2 and Tem1 that are necessary for their localization and for the generation of the asymmetry; (iv) Examine the consequences of disrupting the asymmetry in the Tem1 complex localization on the progression through the cell cycle. Answering these questions will increase our knowledge about the regulation of the exit from mitosis and the mechanisms that control the cell cycle. Since a key function of the MEN is to maintain ploidy, and ploidy is often affected in tumors, our research will also shed light on one of the key initiation steps in tumor formation.'