Kinesin KIF16B Participates in G2/M Transition and Microtubule Dynamics via Aurora A-PLK1 in Oocyte Meiosis

Area of Science:

• Cell Biology
• Reproductive Biology
• Molecular Motors

Background:

• Kinesin-3 family motor proteins, like KIF16B, regulate essential cellular processes including vesicle transport and microtubule dynamics during mitosis.
• The specific role of KIF16B in meiosis, particularly in oocytes, remained largely unexplored.

Purpose of the Study:

• To investigate the function of KIF16B during meiosis in mouse oocytes.
• To elucidate the molecular mechanisms by which KIF16B influences meiotic progression and spindle formation.

Main Methods:

• KIF16B expression analysis throughout the meiotic cell cycle.
• KIF16B depletion studies to assess its impact on meiotic progression.
• Analysis of cell cycle regulators (CDK1, cyclin B1) and spindle assembly.
• Investigation of kinetochore-microtubule (K-MT) attachments and associated signaling pathways (BubR1/Bub3).
• Assessment of KIF16B's interaction with α-tubulin, HDAC6, Ran GTPase, TPX2, Aurora A, and PLK1.

Main Results:

• KIF16B is expressed throughout mouse oocyte meiosis and concentrates on microtubules post-germinal vesicle breakdown.
• KIF16B depletion impairs meiotic progression by inactivating CDK1 and reducing cyclin B1, leading to failed germinal vesicle breakdown.
• Loss of KIF16B results in aberrant spindle phenotypes, misaligned chromosomes, and improper K-MT attachments, causing persistent kinetochore activation of BubR1/Bub3.
• KIF16B knockdown destabilizes α-tubulin via HDAC6 and participates in Ran GTPase-dependent activation of TPX2, influencing Aurora A-PLK1 phosphorylation for spindle assembly.

Conclusions:

• KIF16B plays a critical role in regulating the meiotic G2-M transition and spindle assembly in mouse oocytes.
• KIF16B is essential for meiosis resumption and ensuring accurate chromosome segregation through proper spindle formation and kinetochore-microtubule interactions.