The Mad2 protein plays a key role in the spindle assembly checkpoint (SAC) function. The SAC pathway delays mitotic progression into anaphase until all kinetochores attach to the spindle during mitosis. The formation of the Mad2–p31^comet complex correlates with the completion of spindle attachment and the entry into anaphase during mitosis.

Herein, we showed that dynein intermediate chain 2c (DNCI2c)—a subunit of dynein motor protein—forms an immunocomplex with p31^comet during mitosis. DNCI2c-knockdown resulted in prolonged mitotic arrest in a Mad2-dependent manner. Furthermore, DNCI2c-knockdown-induced mitotic arrest was not rescued by p31^comet overexpression. However, the combination of p31^comet overexpression with the mitotic drug treatment reversed the mitotic arrest in DNCI2c-knockdown. Together, these results indicate that the DNCI2c–p31^comet complex plays an important role in exiting Mad2-dependent SAC.

Mad2 蛋白在纺锤体组装检查点 (SAC) 功能中起着关键作用。SAC 通路延迟有丝分裂进入后期，直到所有着丝粒在有丝分裂期间都附着在纺锤体上。Mad2-p31^彗星复合体的形成与纺锤体附着的完成和有丝分裂期间进入后期相关。

在此，我们展示了动力蛋白中间链 2c (DNCI2c)——动力蛋白运动蛋白的一个亚基——在有丝分裂期间与 p31^彗星形成免疫复合物。DNCI2c 敲低导致以 Mad2 依赖性方式延长有丝分裂停滞。此外，p31^彗星过表达不能挽救 DNCI2c 敲低诱导的有丝分裂停滞。然而，p31^彗星过表达与有丝分裂药物治疗的组合逆转了 DNCI2c 敲低中的有丝分裂停滞。总之，这些结果表明 DNCI2c-p31^彗星复合物在退出依赖于 Mad2 的 SAC 中起着重要作用。