Molecular mechanisms of bipolar spindle assembly in the absence of Kinesin-5/Cut7

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K07694
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Applied biochemistry
• Research Institution: Hiroshima University
• Principal Investigator: Yukawa Masashi 広島大学, 先端物質科学研究科, 特任助教 (50403605)
• Research Collaborator: TODA takashi
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 染色体分配 / 紡錘体 / 微小管 / キネシンモーター / 5型キネシン / 14型キネシン / 微小管ポリメラーゼ / 有糸分裂

Outline of Final Research Achievements

The assembly of a bipolar spindle is necessary to ensure the fidelity of chromosome segregation. In all eukaryotes, spindle formation is driven by the plus-end directed motor kinesin-5. Inactivation of this kinesin causes mitotic arrest with monopolar spindles. Interestingly, simultaneous inactivation of the minus-end directed kinesin-14 restores cell viability in fission yeast. Apparent normal spindle assembly in the absence of both kinesin-5 and kinesin-14 has highlighted the existence of other hitherto unknown factors by which to establish and maintain mitotic bipolar spindles. To uncover these molecules, we have conducted two complementary independent genetic screens. Consequently, we have succeeded in identifying kinesins, microtubule-associated proteins and their regulators.

Free Research Field

細胞分子生物学

Academic Significance and Societal Importance of the Research Achievements

本研究成果により同定に成功した新規紡錘体形成因子はいずれも酵母からヒトまで進化上高度に保存されていることから、高等生物においても類似した紡錘体形成機構が存在すると考えられる。また、これらの新規紡錘体形成因子を阻害することにより、がん細胞の増殖を抑えることができると考えられ、副作用の少ないがん治療薬の開発に繋がることが期待される。