Loss of Kinesin KIF16B Disrupts Organelle Dynamics for Developmental Potential in Oocytes

Kinesin KIF16B, as a molecular motor protein within cells, primarily utilizes energy derived from ATP hydrolysis to transport intracellular cargo along microtubules, thereby participating in material transport, organelle dynamics, and cytoskeletal organization. However, the mechanism by which KIF16B regulates the maturation process of cytoplasm in mouse oocytes remains unclear. This study was to investigate the potential role of KIF16B in modulating organelle dynamics in mouse oocytes. Our findings suggest that depletion of KIF16B impairs oocyte developmental competence following parthenogenesis, implying potential abnormalities in oocyte maturation. We observed that oocytes with diminished KIF16B exhibited disrupted mitochondrial distribution and function, and further analysis revealed that this may be due to KIF16B involvement in p-Drp1 and Fis1-mediated mitochondrial fission. Besides, impaired mitochondrial function also resulted in oxidative stress. Additionally, abnormal distribution of the ER and ER stress were observed in oocytes lacking KIF16B. This was accompanied by elevated expression of ER stress-related genes CHOP and ATF4. Concurrently, KIF16B knockdown affected the distribution and function of the Golgi apparatus, leading to abnormalities in Golgi-based vesicular transport processes. In summary, our data suggest that the kinesin KIF16B modulates organelle dynamics during oocyte maturation.