Vesicular trafficking plays a role in centriole disengagement and duplication

Shuwei Xie, James B. Reinecke, Trey Farmer, Kriti Bahl, Ivana Yeow, Benjamin J. Nichols, Tiffany A. McLamarrah, Naava Naslavsky, Gregory C. Rogers, Steve Caplan

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Centrosomes are the major microtubule-nucleating and microtubule-organizing centers of cells and play crucial roles in microtubule anchoring, organelle positioning, and ciliogenesis. At the centrosome core lies a tightly associated or “engaged” mother-daughter centriole pair. During mitotic exit, removal of centrosomal proteins pericentrin and Cep215 promotes “disengagement” by the dissolution of intercentriolar linkers, ensuring a single centriole duplication event per cell cycle. Herein, we explore a new mechanism involving vesicular trafficking for the removal of centrosomal Cep215. Using small interfering RNA and CRISPR/Cas9 gene-edited cells, we show that the endocytic protein EHD1 regulates Cep215 transport from centrosomes to the spindle midbody, thus facilitating disengagement and duplication. We demonstrate that EHD1 and Cep215 interact and show that Cep215 displays increased localization to vesicles containing EHD1 during mitosis. Moreover, Cep215-contain-ing vesicles are positive for internalized transferrin, demonstrating their endocytic origin. Thus, we describe a novel relationship between endocytic trafficking and the centrosome cycle, whereby vesicles of endocytic origin are used to remove key regulatory proteins from centrosomes to control centriole duplication.

Original languageEnglish (US)
Pages (from-to)2622-2631
Number of pages10
JournalMolecular biology of the cell
Issue number22
StatePublished - Nov 1 2018

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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