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Çaydaşı, Ayşe Koca

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Ayşe Koca

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Çaydaşı

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Çaydaşı, Ayşe Koca

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2017 - 201912020 - 20232

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Researcher Of Publications: search.filters.isAuthorOfPublication.b1711b4f-0394-4cb3-ae9f-a35d78552bde

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    SWR1 chromatin remodeling complex prevents mitotic slippage during spindle position checkpoint arrest
    (American Society for Cell Biology, 2023) Khmelinskii, Anton; Darieva, Zoulfia; Kurtulmus, Bahtiyar; Knop, Michael; Pereira, Gislene; Department of Molecular Biology and Genetics; Çaydaşı, Ayşe Koca; Faculty Member; Department of Molecular Biology and Genetics; College of Sciences; 252978
    Faithful chromosome segregation in budding yeast requires correct positioning of the mitotic spindle along the mother to daughter cell polarity axis. When the anaphase spindle is not correctly positioned, a surveillance mechanism, named as the spindle position checkpoint (SPOC), prevents the progression out of mitosis until correct spindle positioning is achieved. How SPOC works on a molecular level is not well understood. Here we performed a genome-wide genetic screen to search for components required for SPOC. We identified the SWR1 chromatin-remodeling complex (SWR1-C) among several novel factors that are essential for SPOC integrity. Cells lacking SWR1-C were able to activate SPOC upon spindle misorientation but underwent mitotic slippage upon prolonged SPOC arrest. This mitotic slippage required the Cdc14-early anaphase release pathway and other factors including the SAGA (Spt-Ada-Gcn5 acetyltransferase) histone acetyltransferase complex, proteasome components and the mitotic cyclin-dependent kinase inhibitor Sic1. Together, our data establish a novel link between SWR1-C chromatin remodeling and robust checkpoint arrest in late anaphase.
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    PublicationOpen Access
    Temporal and compartment-specific signals coordinate mitotic exit with spindle position
    (Nature Publishing Group (NPG), 2017) Khmelinskii, Anton; Duenas-Sanchez, Rafael; Kurtulmus, Bahtiyar; Knop, Michael; Pereira, Gislene; Department of Molecular Biology and Genetics; Çaydaşı, Ayşe Koca; Faculty Member; Department of Molecular Biology and Genetics; College of Sciences; 252978
    The spatiotemporal control of mitotic exit is crucial for faithful chromosome segregation during mitosis. In budding yeast, the mitotic exit network (MEN) drives cells out of mitosis, whereas the spindle position checkpoint (SPOC) blocks MEN activity when the anaphase spindle is mispositioned. How the SPOC operates at a molecular level remains unclear. Here, we report novel insights into how mitotic signalling pathways orchestrate chromosome segregation in time and space. We establish that the key function of the central SPOC kinase, Kin4, is to counterbalance MEN activation by the cdc fourteen early anaphase release (FEAR) network in the mother cell compartment. Remarkably, Kin4 becomes dispensable for SPOC function in the absence of FEAR. Cells lacking both FEAR and Kin4 show that FEAR contributes to mitotic exit through regulation of the SPOC component Bfa1 and the MEN kinase Cdc15. Furthermore, we uncover controls that specifically promote mitotic exit in the daughter cell compartment.
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    PublicationOpen Access
    Protein phosphatase 1 in association with Bud14 inhibits mitotic exit in Saccharomyces cerevisiae
    (eLife Sciences Publications, 2021) Department of Molecular Biology and Genetics; Çaydaşı, Ayşe Koca; Kocakaplan, Dilara; Karabürk, Hüseyin; Dilege, Cansu; Kırdök, İdil; Bektaş, Şeyma Nur; Faculty Member; Department of Molecular Biology and Genetics; Graduate School of Sciences and Engineering; College of Engineering; 252978; N/A; N/A; N/A; N/A; N/A
    Mitotic exit in budding yeast is dependent on correct orientation of the mitotic spindle along the cell polarity axis. When accurate positioning of the spindle fails, a surveillance mechanism named the Spindle Position Checkpoint (SPOC) prevents cells from exiting mitosis. Mutants with a defective SPOC become multinucleated and lose their genomic integrity. Yet, a comprehensive understanding of the SPOC mechanism is missing. In this study, we identified the type 1 protein phosphatase, Glc7, in association with its regulatory protein Bud14 as a novel checkpoint component. We further showed that Glc7-Bud14 promotes dephosphorylation of the SPOC effector protein Bfa1. Our results suggest a model in which two mechanisms act in parallel for a robust checkpoint response: first, the SPOC kinase Kin4 isolates Bfa1 away from the inhibitory kinase Cdc5 and second, Glc7-Bud14 dephosphorylates Bfa1 to fully activate the checkpoint effector.