| 时间 |
2023年11月7日，12:00-13:00 |
| 地点 |
生物医学馆E203 |
| 报告人 |
陈广涵（直博三年级） |
| 题目 | Neurons dispose of hyperactive kinesin into glial cells for clearance |
| 摘要 | Microtubule-based kinesin motor proteins are crucial for intracellular transport. However, the mechanisms that govern kinesin hyperactivation remains elusive. This study investigated the impact of a constitutively active ciliary kinesin, OSM-3CA, on sensory cilia in C. elegans. Surprisingly, we found that OSM-3CA was absent from cilia but underwent disposal through membrane abscission at the tips of aberrant neurites. Neighboring glial cells engulf and eliminate the released OSM-3CA, a process that depends on the engulfment receptor CED-1. Through genetic suppressor screens, we identified intragenic mutations in the OSM-3CA motor domain and mutations inhibiting the ciliary kinase DYF-5, both of which restored normal cilia in OSM-3CA animals. We showed that conformational changes in OSM-3CA prevent its entry into cilia, and OSM-3CA disposal requires its hyperactivity. We provide evidence that neurons also dispose of hyperactive kinesin-1 resulting from a clinic variant associated with amyotrophic lateral sclerosis, suggesting a widespread mechanism for regulating hyperactive kinesin. |
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