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The yeast centrosome translates the positional information of the anaphase spindle into a cell cycle signal
Authors:Maekawa Hiromi  Priest Claire  Lechner Johannes  Pereira Gislene  Schiebel Elmar
Affiliation:1.Zentrum für Molekulare Biologie and 2.Biochemie-Zentrum, Universität Heidelberg, 69120 Heidelberg, Germany; 3.The Paterson Institute for Cancer Research, Manchester M20 4BX, UK; 4.German Cancer Research Centre, 69120 Heidelberg, Germany
Abstract:The spindle orientation checkpoint (SPOC) of budding yeast delays mitotic exit when cytoplasmic microtubules (MTs) are defective, causing the spindle to become misaligned. Delay is achieved by maintaining the activity of the Bfa1-Bub2 guanosine triphosphatase-activating protein complex, an inhibitor of mitotic exit. In this study, we show that the spindle pole body (SPB) component Spc72, a transforming acidic coiled coil-like molecule that interacts with the gamma-tubulin complex, recruits Kin4 kinase to both SPBs when cytoplasmic MTs are defective. This allows Kin4 to phosphorylate the SPB-associated Bfa1, rendering it resistant to inactivation by Cdc5 polo kinase. Consistently, forced targeting of Kin4 to both SPBs delays mitotic exit even when the anaphase spindle is correctly aligned. Moreover, we present evidence that Spc72 has an additional function in SPOC regulation that is independent of the recruitment of Kin4. Thus, Spc72 provides a missing link between cytoplasmic MT function and components of the SPOC.
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