1. A dynamical model of the spindle position checkpoint
MEN and SPOC. (A) Schematic representation of MEN and SPOC pathways. Tem1 triggers the MEN cascade by promoting SPB recruitment of Cdc15 kinase, which activates Dbf2–Mob1 at the SPBs. Dbf2–Mob1 promotes the full release of Cdc14 from the nucleolus into the cytoplasm. Fully released Cdc14 inactivates the mitotic cyclin/Cdk and reverses the Cdk‐dependent phosphorylation of several Cdk substrates, hence providing mitotic exit (Visintin et al, 1998; Jaspersen et al, 1999; Stegmeier and Amon, 2004). Misalignment of the mitotic spindle activates Bfa1–Bub2 via Kin4, hence Tem1 is inhibited. Kin4 is under tight control: Phosphorylation of the conserved threonine (T209) residue within Kin4's activation loop by the bud neck kinase Elm1 is essential for Kin4 catalytic activity (Caydasi et al, 2010b; Moore et al, 2010). Rts1, B type regulatory subunit of the protein phosphatase 2A (PP2A), provides proper Kin4 localization at the SPBs and at the mother cell cortex by promoting Kin4 dephosphorylation (Chan and Amon, 2009; Caydasi et al, 2010b). Daughter‐specific protein Lte1 inactivates Kin4 and excludes it from the dSPB during an unperturbed anaphase, counteracting Rts1 (Bertazzi et al, 2011; Falk et al, 2011). (B) Localization of the SPOC components (colored in A) in an anaphase cell with misaligned (left panel) and correctly aligned (right panel) spindle. Protein color coding is consistent in (A, B).
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Mol Syst Biol, Volume: 8, Issue: 1, First published: 08 May 2012, DOI: ( /msb )