論文

査読有り
2017年12月

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
  • Masashi Yukawa
  • ,
  • Tomoki Kawakami
  • ,
  • Masaki Okazaki
  • ,
  • Kazunori Kume
  • ,
  • Ngang Heok Tang
  • ,
  • Takashi Toda

28
25
開始ページ
3647
終了ページ
3659
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1091/mbc.E17-08-0497
出版者・発行元
AMER SOC CELL BIOLOGY

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/TACCAlp14/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.

Web of Science ® 被引用回数 : 17

リンク情報
DOI
https://doi.org/10.1091/mbc.E17-08-0497
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000416513200009&DestApp=WOS_CPL
ID情報
  • DOI : 10.1091/mbc.E17-08-0497
  • ISSN : 1059-1524
  • eISSN : 1939-4586
  • Web of Science ID : WOS:000416513200009

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