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@ARTICLE{Maekawa:179938,
      author       = {H. Maekawa and S. Jiangyan and K. Takegawa and G.
                      Pereira$^*$},
      title        = {{SIN}-{L}ike {P}athway {K}inases {R}egulate the {E}nd of
                      {M}itosis in the {M}ethylotrophic {Y}east {O}gataea
                      polymorpha.},
      journal      = {Cells},
      volume       = {11},
      number       = {9},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2022-00987},
      pages        = {1519},
      year         = {2022},
      note         = {#LA:A180#},
      abstract     = {The mitotic exit network (MEN) is a conserved signalling
                      pathway essential for the termination of mitosis in the
                      budding yeast Saccharomyces cerevisiae. All MEN components
                      are highly conserved in the methylotrophic budding yeast
                      Ogataea polymorpha, except for Cdc15 kinase. Instead, we
                      identified two essential kinases OpHcd1 and OpHcd2
                      (homologue candidate of ScCdc15) that are homologous to
                      SpSid1 and SpCdc7, respectively, components of the septation
                      initiation network (SIN) of the fission yeast
                      Schizosaccharomyces pombe. Conditional mutants for OpHCD1
                      and OpHCD2 exhibited significant delay in late anaphase and
                      defective cell separation, suggesting that both genes have
                      roles in mitotic exit and cytokinesis. Unlike Cdc15 in S.
                      cerevisiae, the association of OpHcd1 and OpHcd2 with the
                      yeast centrosomes (named spindle pole bodies, SPBs) is
                      restricted to the SPB in the mother cell body. SPB
                      localisation of OpHcd2 is regulated by the status of OpTem1
                      GTPase, while OpHcd1 requires the polo-like kinase OpCdc5 as
                      well as active Tem1 to ensure the coordination of mitotic
                      exit (ME) signalling and cell cycle progression. Our study
                      suggests that the divergence of molecular mechanisms to
                      control the ME-signalling pathway as well as the loss of
                      Sid1/Hcd1 kinase in the MEN occurred relatively recently
                      during the evolution of budding yeast.},
      keywords     = {Cdc15 kinase (Other) / Cdc5 kinase (Other) / Ogataea
                      polymorpha (Other) / SPB (Other) / mitotic exit network
                      (Other) / septation initiation network (Other)},
      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:35563825},
      doi          = {10.3390/cells11091519},
      url          = {https://inrepo02.dkfz.de/record/179938},
}