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IFT proteins interact with HSET to promote supernumerary centrosome clustering in mitosis
Author(s) -
Vitre Benjamin,
Taulet Nicolas,
Guesdon Audrey,
Douanier Audrey,
Dosdane Aurelie,
Cisneros Melanie,
Maurin Justine,
Hettinger Sabrina,
Anguille Christelle,
Taschner Michael,
Lorentzen Esben,
Delaval Benedicte
Publication year - 2020
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201949234
Subject(s) - centrosome , microbiology and biotechnology , mitosis , centrosome cycle , biology , genetics , cell cycle , gene
Centrosome amplification is a hallmark of cancer, and centrosome clustering is essential for cancer cell survival. The mitotic kinesin HSET is an essential contributor to this process. Recent studies have highlighted novel functions for intraflagellar transport (IFT) proteins in regulating motors and mitotic processes. Here, using siRNA knock‐down of various IFT proteins or AID‐inducible degradation of endogenous IFT88 in combination with small‐molecule inhibition of HSET, we show that IFT proteins together with HSET are required for efficient centrosome clustering. We identify a direct interaction between the kinesin HSET and IFT proteins, and we define how IFT proteins contribute to clustering dynamics during mitosis using high‐resolution live imaging of centrosomes. Finally, we demonstrate the requirement of IFT88 for efficient centrosome clustering in a variety of cancer cell lines naturally harboring supernumerary centrosomes and its importance for cancer cell proliferation. Overall, our data unravel a novel role for the IFT machinery in centrosome clustering during mitosis in cells harboring supernumerary centrosomes.