Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression

Abstract Plk1 is a key mitotic kinase that localizes to distinct subcellular structures to promote accurate mitotic progression. Plk1 recruitment depends on direct interaction between polo-box domain (PBD) on Plk1 and PBD binding motif (PBD BM) on the interactors. However, recent study showed that P...

Full description

Saved in:
Bibliographic Details
Main Authors: Chunlin Song, Mingzhe Zhang, Thomas Kruse, Mads Harder Møller, Blanca López-Méndez, Yuqing Zhang, Yujing Zhai, Ying Wang, Tingting Lei, Arminja N. Kettenbach, Jakob Nilsson, Gang Zhang
Format: Article
Language:English
Published: Nature Portfolio 2024-11-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-024-07205-2
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850194737679564800
author Chunlin Song
Mingzhe Zhang
Thomas Kruse
Mads Harder Møller
Blanca López-Méndez
Yuqing Zhang
Yujing Zhai
Ying Wang
Tingting Lei
Arminja N. Kettenbach
Jakob Nilsson
Gang Zhang
author_facet Chunlin Song
Mingzhe Zhang
Thomas Kruse
Mads Harder Møller
Blanca López-Méndez
Yuqing Zhang
Yujing Zhai
Ying Wang
Tingting Lei
Arminja N. Kettenbach
Jakob Nilsson
Gang Zhang
author_sort Chunlin Song
collection DOAJ
description Abstract Plk1 is a key mitotic kinase that localizes to distinct subcellular structures to promote accurate mitotic progression. Plk1 recruitment depends on direct interaction between polo-box domain (PBD) on Plk1 and PBD binding motif (PBD BM) on the interactors. However, recent study showed that PBD BM alone is not enough for stable binding between CENP-U and Plk1 highlighting the complexity of the interaction which warrants further investigation. An important interactor for Plk1 during mitosis is the checkpoint protein BubR1. Plk1 bound to BubR1 via PBD interaction with pT620 phosphorylates BubR1 S676/T680 to promote BubR1-PP2A/B56 interaction. The BubR1-PP2A/B56 complex counteracts the destablizing effect on kinetochore-microtubule attachments by mitotic kinases to promote mitotic progression. Here we show that Plk1 phosphorylates T600/T608 on BubR1 and the double phosphorylation is critical for BubR1-Plk1 interaction. A similar mechanism for Plk1-Bub1 interaction also exists indicating a general principle for Plk1 kinetochore recruitment through self-priming. Mechanistically preventing BubR1 T600/T608 phosphorylation impairs chromosome congression and checkpoint silencing by reducing Plk1 and PP2A/B56 binding to BubR1. Increasing the binding affinity towards Plk1 and PP2A/B56 in BubR1 through protein engineering bypasses the requirement of T600/T608 phosphorylation for mitotic progression. These results reveal a new layer of regulation for accurate mitotic progression.
format Article
id doaj-art-ece991e00281497d80b9a72cab0b6158
institution OA Journals
issn 2399-3642
language English
publishDate 2024-11-01
publisher Nature Portfolio
record_format Article
series Communications Biology
spelling doaj-art-ece991e00281497d80b9a72cab0b61582025-08-20T02:13:55ZengNature PortfolioCommunications Biology2399-36422024-11-017111110.1038/s42003-024-07205-2Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progressionChunlin Song0Mingzhe Zhang1Thomas Kruse2Mads Harder Møller3Blanca López-Méndez4Yuqing Zhang5Yujing Zhai6Ying Wang7Tingting Lei8Arminja N. Kettenbach9Jakob Nilsson10Gang Zhang11The Cancer Institute, The Affiliated Hospital of Qingdao University, Qingdao UniversityThe Cancer Institute, The Affiliated Hospital of Qingdao University, Qingdao UniversityNovo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of CopenhagenNovo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of CopenhagenNovo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of CopenhagenThe Cancer Institute, The Affiliated Hospital of Qingdao University, Qingdao UniversitySchool of Public Health, Qingdao UniversitySchool of Public Health, Qingdao UniversityThe Cancer Institute, The Affiliated Hospital of Qingdao University, Qingdao UniversityDepartment of Biochemistry and Cell Biology, Geisel School of Medicine at Dartmouth CollegeNovo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of CopenhagenThe Cancer Institute, The Affiliated Hospital of Qingdao University, Qingdao UniversityAbstract Plk1 is a key mitotic kinase that localizes to distinct subcellular structures to promote accurate mitotic progression. Plk1 recruitment depends on direct interaction between polo-box domain (PBD) on Plk1 and PBD binding motif (PBD BM) on the interactors. However, recent study showed that PBD BM alone is not enough for stable binding between CENP-U and Plk1 highlighting the complexity of the interaction which warrants further investigation. An important interactor for Plk1 during mitosis is the checkpoint protein BubR1. Plk1 bound to BubR1 via PBD interaction with pT620 phosphorylates BubR1 S676/T680 to promote BubR1-PP2A/B56 interaction. The BubR1-PP2A/B56 complex counteracts the destablizing effect on kinetochore-microtubule attachments by mitotic kinases to promote mitotic progression. Here we show that Plk1 phosphorylates T600/T608 on BubR1 and the double phosphorylation is critical for BubR1-Plk1 interaction. A similar mechanism for Plk1-Bub1 interaction also exists indicating a general principle for Plk1 kinetochore recruitment through self-priming. Mechanistically preventing BubR1 T600/T608 phosphorylation impairs chromosome congression and checkpoint silencing by reducing Plk1 and PP2A/B56 binding to BubR1. Increasing the binding affinity towards Plk1 and PP2A/B56 in BubR1 through protein engineering bypasses the requirement of T600/T608 phosphorylation for mitotic progression. These results reveal a new layer of regulation for accurate mitotic progression.https://doi.org/10.1038/s42003-024-07205-2
spellingShingle Chunlin Song
Mingzhe Zhang
Thomas Kruse
Mads Harder Møller
Blanca López-Méndez
Yuqing Zhang
Yujing Zhai
Ying Wang
Tingting Lei
Arminja N. Kettenbach
Jakob Nilsson
Gang Zhang
Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression
Communications Biology
title Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression
title_full Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression
title_fullStr Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression
title_full_unstemmed Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression
title_short Self-priming of Plk1 binding to BubR1 ensures accurate mitotic progression
title_sort self priming of plk1 binding to bubr1 ensures accurate mitotic progression
url https://doi.org/10.1038/s42003-024-07205-2
work_keys_str_mv AT chunlinsong selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT mingzhezhang selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT thomaskruse selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT madshardermøller selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT blancalopezmendez selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT yuqingzhang selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT yujingzhai selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT yingwang selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT tingtinglei selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT arminjankettenbach selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT jakobnilsson selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression
AT gangzhang selfprimingofplk1bindingtobubr1ensuresaccuratemitoticprogression