Cep57 and Cep57L1 maintain centriole engagement in interphase to ensure centriole duplication cycle.


Journal

The Journal of cell biology
ISSN: 1540-8140
Titre abrégé: J Cell Biol
Pays: United States
ID NLM: 0375356

Informations de publication

Date de publication:
01 03 2021
Historique:
received: 21 05 2020
revised: 27 10 2020
accepted: 15 12 2020
entrez: 25 1 2021
pubmed: 26 1 2021
medline: 10 9 2021
Statut: ppublish

Résumé

Centrioles duplicate in interphase only once per cell cycle. Newly formed centrioles remain associated with their mother centrioles. The two centrioles disengage at the end of mitosis, which licenses centriole duplication in the next cell cycle. Therefore, timely centriole disengagement is critical for the proper centriole duplication cycle. However, the mechanisms underlying centriole engagement during interphase are poorly understood. Here, we show that Cep57 and Cep57L1 cooperatively maintain centriole engagement during interphase. Codepletion of Cep57 and Cep57L1 induces precocious centriole disengagement in interphase without compromising cell cycle progression. The disengaged daughter centrioles convert into centrosomes during interphase in a Plk1-dependent manner. Furthermore, the centrioles reduplicate and the centriole number increases, which results in chromosome segregation errors. Overall, these findings demonstrate that the maintenance of centriole engagement by Cep57 and Cep57L1 during interphase is crucial for the tight control of centriole copy number and thus for proper chromosome segregation.

Identifiants

pubmed: 33492359
pii: 211711
doi: 10.1083/jcb.202005153
pmc: PMC7836272
pii:
doi:

Substances chimiques

CEP57 protein, human 0
Cell Cycle Proteins 0
Microtubule-Associated Proteins 0
Nuclear Proteins 0
Proto-Oncogene Proteins 0
Protein Serine-Threonine Kinases EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2021 Ito et al.

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Auteurs

Kei K Ito (KK)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

Koki Watanabe (K)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

Haruki Ishida (H)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

Kyohei Matsuhashi (K)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

Takumi Chinen (T)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

Shoji Hata (S)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

Daiju Kitagawa (D)

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan.

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Classifications MeSH