A microtubule polymerase cooperates with the kinesin-6 motor and a microtubule cross-linker to promote bipolar spindle assembly in the absence of kinesin-5 and kinesin-14 in fission yeast

Molecular Biology of the Cell 28 巻 25 号 3647-3659 頁 2017-12-01 発行
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タイトル ( eng )
A microtubule polymerase cooperates with the kinesin-6 motor and a microtubule cross-linker to promote bipolar spindle assembly in the absence of kinesin-5 and kinesin-14 in fission yeast
作成者
Kawakami Tomoki
Okazaki Masaki
Ngang Heok Tang
収録物名
Molecular Biology of the Cell
28
25
開始ページ 3647
終了ページ 3659
抄録
Accurate chromosome segregation relies on the bipolar mitotic spindle. In many eukaryotes, spindle formation is driven by the plus-end–directed motor kinesin-5 that generates outward force to establish spindle bipolarity. Its inhibition leads to the emergence of monopolar spindles with mitotic arrest. Intriguingly, simultaneous inactivation of the minus-end–directed motor kinesin-14 restores spindle bipolarity in many systems. Here we show that in fission yeast, three independent pathways contribute to spindle bipolarity in the absence of kinesin-5/Cut7 and kinesin-14/Pkl1. One is kinesin-6/Klp9 that engages with spindle elongation once short bipolar spindles assemble. Klp9 also ensures the medial positioning of anaphase spindles to prevent unequal chromosome segregation. Another is the Alp7/TACC-Alp14/TOG microtubule polymerase complex. Temperature-sensitive alp7cut7pkl1 mutants are arrested with either monopolar or very short spindles. Forced targeting of Alp14 to the spindle pole body is sufficient to render alp7cut7pkl1 triply deleted cells viable and promote spindle assembly, indicating that Alp14-mediated microtubule polymerization from the nuclear face of the spindle pole body could generate outward force in place of Cut7 during early mitosis. The third pathway involves the Ase1/PRC1 microtubule cross-linker that stabilizes antiparallel microtubules. Our study, therefore, unveils multifaceted interplay among kinesin-dependent and -independent pathways leading to mitotic bipolar spindle assembly.
内容記述
This work was supported by the Japan Society for the Promotion of Science (JSPS) (KAKENHI Scientific Research [A] 16H02503 to T.T., a Challenging Exploratory Research grant 16K14672 to T.T., Scientific Research [C] 16K07694 to M.Y.), the Naito Foundation (T.T.), and the Uehara Memorial Foundation (T.T.).
言語
英語
資源タイプ 学術雑誌論文
出版者
The American Society for Cell Biology
発行日 2017-12-01
権利情報
© 2017 Yukawa et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
出版タイプ Version of Record(出版社版。早期公開を含む)
アクセス権 オープンアクセス
収録物識別子
[ISSN] 1059-1524
[ISSN] 1939-4586
[DOI] 10.1091/mbc.e17-08-0497
[DOI] https://doi.org/10.1091/mbc.e17-08-0497
[PMID] 29021344