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Mammalian CLASPs are required for mitotic spindle organization and kinetochore alignment
Author(s) -
MimoriKiyosue Yuko,
Grigoriev Ilya,
Sasaki Hiroyuki,
Matsui Chiyuki,
Akhmanova Anna,
Tsukita Shoichiro,
Vorobjev Ivan
Publication year - 2006
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2006.00990.x
Subject(s) - kinetochore , microbiology and biotechnology , metaphase , biology , mitosis , microtubule , anaphase , aurora b kinase , astral microtubules , spindle apparatus , interphase , cytokinesis , advanced spaceborne thermal emission and reflection radiometer , mitotic exit , cell division , genetics , cell , cell cycle , chromosome , physics , satellite , astronomy , gene
CLASP1 and CLASP2 are homologous mammalian proteins, which associate with the ends of growing microtubules, as well as the cell cortex and the kinetochores of mitotic chromosomes. Previous studies have shown that in interphase cells CLASPs can attach microtubule plus ends to the cortex and stabilize them by repeatedly rescuing them from depolymerization. Here we show that CLASP1 and 2 play similar and redundant roles in organizing the mitotic apparatus in HeLa cells. Simultaneous depletion of both CLASPs causes mitotic spindle defects and a significant metaphase delay, which often results in abnormal exit from mitosis. Metaphase delay is associated with decreased kinetochore tension, increased kinetochore oscillations and more rapid microtubule growth. We show that the association of CLASP2 with the kinetochores relies on its C‐terminal domain, but is independent of microtubules or association with CLIP‐170. We propose that CLASPs exhibit at the kinetochores an activity similar to that at the cortex, providing apparent stabilization of microtubules by locally reducing the amplitude of growth/shortening episodes at the microtubule ends. This local stabilization of microtubules is essential for the formation of normal metaphase spindle, completion of anaphase and cytokinesis.