The Cep57-pericentrin module organizes PCM expansion and centriole engagement.
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
25 02 2019
25 02 2019
Historique:
received:
30
11
2017
accepted:
31
01
2019
entrez:
27
2
2019
pubmed:
26
2
2019
medline:
18
4
2019
Statut:
epublish
Résumé
Centriole duplication occurs once per cell cycle to ensure robust formation of bipolar spindles and chromosome segregation. Each newly-formed daughter centriole remains connected to its mother centriole until late mitosis. The disengagement of the centriole pair is required for centriole duplication. However, the mechanisms underlying centriole engagement remain poorly understood. Here, we show that Cep57 is required for pericentriolar material (PCM) organization that regulates centriole engagement. Depletion of Cep57 causes PCM disorganization and precocious centriole disengagement during mitosis. The disengaged daughter centrioles acquire ectopic microtubule-organizing-center activity, which results in chromosome mis-segregation. Similar defects are observed in mosaic variegated aneuploidy syndrome patient cells with cep57 mutations. We also find that Cep57 binds to the well-conserved PACT domain of pericentrin. Microcephaly osteodysplastic primordial dwarfism disease pericentrin mutations impair the Cep57-pericentrin interaction and lead to PCM disorganization. Together, our work demonstrates that Cep57 provides a critical interface between the centriole core and PCM.
Identifiants
pubmed: 30804344
doi: 10.1038/s41467-019-08862-2
pii: 10.1038/s41467-019-08862-2
pmc: PMC6389942
doi:
Substances chimiques
Antigens
0
CEP57 protein, human
0
Microtubule-Associated Proteins
0
Nuclear Proteins
0
pericentrin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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