4.7 Article

Channel Nucleoporins Recruit PLK-1 to Nuclear Pore Complexes to Direct Nuclear Envelope Breakdown in C-elegans

期刊

DEVELOPMENTAL CELL
卷 43, 期 2, 页码 157-+

出版社

CELL PRESS
DOI: 10.1016/j.devcel.2017.09.019

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资金

  1. NIH Office of Research [P40 OD010440]
  2. La Ligue Nationale contre le Cancer [IP/SC-13379]
  3. French National Research Agency [ANR-2012-BSV2-0001-01, ANR-2012-BSV2-0008-01]
  4. Fondation pour la Recherche Medicale (Foundation for Medical Research) Equipes [FRM DEQ20140329538, DEQ20150734355]
  5. Labex Who am I?'' Laboratory of Excellence [ANR-11-LABX-0071]
  6. French Government [ANR-11-IDEX-0005-01]
  7. France-BioImaging [ANR-10-INBS-04]
  8. NIH [GM074215]
  9. Ministry of Research

向作者/读者索取更多资源

In animal cells, nuclear envelope breakdown (NEBD) is required for proper chromosome segregation. Whereas mitotic kinases have been implicated in NEBD, how they coordinate their activity to trigger this event is unclear. Here, we show that both in human cells and Caenorhabditis elegans, the Polo-like kinase 1 (PLK-1) is recruited to the nuclear pore complexes, just prior to NEBD, through its Polo-box domain (PBD). We provide evidence that PLK-1 localization to the nuclear envelope (NE) is required for efficient NEBD. We identify the central channel nucleoporins NPP-1/Nup58, NPP-4/Nup54, and NPP-11/Nup62 as the critical factors anchoring PLK-1 to the NE in C. elegans. In particular, NPP-1, NPP-4, and NPP-11 primed at multiple Polo-docking sites by Cdk1 and PLK-1 itself physically interact with the PLK-1 PBD. We conclude that nucleoporins play an unanticipated regulatory role in NEBD, by recruiting PLK-1 to the NE thereby facilitating phosphorylation of critical downstream targets.

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