Autophagy starts with the initiation and nucleation of isolation membranes, which further expand and seal to form autophagosomes. The regulation of isolation membrane closure remains poorly understood. CK1δ is a member of the casein kinase I family of serine/threonine specific kinases. Although CK1δ is reported to be involved in various cellular processes, its role in autophagy is unknown. Here, we show that CK1δ regulates the progression of autophagy from the formation of isolation membranes to autophagosome closure, and is essential for macroautophagy. CK1δ depletion results in impaired autophagy flux and the accumulation of unsealed isolation membranes. The association of LC3 with ATG9A, ATG14L, and ATG16L1 was found to be increased in CK1δ-depleted cells. The role of CK1δ in autophagosome completion appears to be conserved between yeasts and humans. Our data reveal a key role for CK1δ/Hrr25 in autophagosome completion.

自噬从隔离膜的起始和成核开始，然后进一步膨胀和密封形成自噬体。隔离膜封闭的规则仍然知之甚少。CK1δ是酪氨酸激酶I家族的丝氨酸/苏氨酸特异性激酶的成员。尽管据报道CK1δ参与各种细胞过程，但其在自噬中的作用尚不清楚。在这里，我们表明CK1δ调节自噬从隔离膜的形成到自噬体封闭的进展，并且对于自噬是必不可少的。CK1δ耗竭会导致自噬通量受损和未密封的隔离膜积聚。发现LC3与ATG9A，ATG14L和ATG16L1的关联在CK1δ缺失的细胞中增加。CK1δ在自噬体完成中的作用似乎在酵母和人之间是保守的。我们的数据揭示了CK1δ/ Hrr25在自噬完成中的关键作用。