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@ARTICLE{Rathi:182432,
      author       = {S. Rathi and I. Polat and G. Pereira$^*$},
      title        = {{T}he budding yeast {GSK}-3 homologue {M}ck1 is an
                      essential component of the spindle position checkpoint.},
      journal      = {Open biology},
      volume       = {12},
      number       = {11},
      issn         = {2046-2441},
      address      = {London},
      publisher    = {Royal Society Publishing},
      reportid     = {DKFZ-2022-02641},
      pages        = {220203},
      year         = {2022},
      note         = {DKFZ-ZMBH Alliance / #LA:A180#},
      abstract     = {The spindle position checkpoint (SPOC) is a mitotic
                      surveillance mechanism in Saccharomyces cerevisiae that
                      prevents cells from completing mitosis in response to
                      spindle misalignment, thereby contributing to genomic
                      integrity. The kinase Kin4, one of the most downstream SPOC
                      components, is essential to stop the mitotic exit network
                      (MEN), a signalling pathway that promotes the exit from
                      mitosis and cell division. Previous work, however, suggested
                      that a Kin4-independent pathway contributes to SPOC, yet the
                      underlying mechanisms remain elusive. Here, we established
                      the glycogen-synthase-kinase-3 (GSK-3) homologue Mck1, as a
                      novel component that works independently of Kin4 to engage
                      SPOC. Our data indicate that both Kin4 and Mck1 work in
                      parallel to counteract MEN activation by the Cdc14 early
                      anaphase release (FEAR) network. We show that Mck1's
                      function in SPOC is mediated by the pre-replication complex
                      protein and mitotic cyclin-dependent kinase (M-Cdk)
                      inhibitor, Cdc6, which is degraded in a Mck1-dependent
                      manner prior to mitosis. Moderate overproduction of Cdc6
                      phenocopies MCK1 deletion and causes SPOC deficiency via its
                      N-terminal, M-Cdk inhibitory domain. Our data uncover an
                      unprecedented role of GSK-3 kinases in coordinating spindle
                      orientation with cell cycle progression.},
      keywords     = {Humans / Saccharomyces cerevisiae Proteins: genetics /
                      Glycogen Synthase Kinase 3: genetics / Glycogen Synthase
                      Kinase 3: metabolism / Spindle Apparatus: metabolism /
                      Saccharomycetales: metabolism / Protein Serine-Threonine
                      Kinases / Phosphorylation / Saccharomyces cerevisiae:
                      genetics / Mitosis / Cell Cycle Proteins: metabolism /
                      Protein Tyrosine Phosphatases: genetics / Protein Tyrosine
                      Phosphatases: metabolism / Cdc6 (Other) / MCK1 (Other) /
                      budding yeast (Other) / cell division (Other) / checkpoint
                      control (Other) / mitotic exit (Other) / Saccharomyces
                      cerevisiae Proteins (NLM Chemicals) / Glycogen Synthase
                      Kinase 3 (NLM Chemicals) / Protein Serine-Threonine Kinases
                      (NLM Chemicals) / Cell Cycle Proteins (NLM Chemicals) /
                      CDC14 protein, S cerevisiae (NLM Chemicals) / Protein
                      Tyrosine Phosphatases (NLM Chemicals) / MCK1 protein, S
                      cerevisiae (NLM Chemicals)},
      cin          = {A180},
      ddc          = {570},
      cid          = {I:(DE-He78)A180-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36321416},
      doi          = {10.1098/rsob.220203},
      url          = {https://inrepo02.dkfz.de/record/182432},
}