Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, California, USA.
Autophagy. 2023 Jan;19(1):358-359. doi: 10.1080/15548627.2022.2074614. Epub 2022 May 15.
A recent screen of the deletion library implicated End3 in autophagy of the endoplasmic reticulum (ER). Together with Pan1, End3 coordinates endocytic site initiation with the localized assembly of branching actin filaments that promotes invagination of endocytic pits. Oxysterol binding proteins function as an inter-organelle bridge by interacting with VAP proteins on the cortical ER and type I myosins on the endocytic pit. These proteins not only promote localized actin assembly at contact sites, they are required for ER autophagy as well. We propose that localized actin polymerization can push the edge of an ER sheet from the cell cortex toward the site of autophagosome assembly near the vacuole.
最近对缺失文库的筛选表明 End3 参与内质网 (ER) 的自噬。End3 与 Pan1 一起协调内吞位点的起始与分支肌动蛋白丝的局部组装,促进内吞凹陷的凹陷。氧化固醇结合蛋白通过与皮质 ER 上的 VAP 蛋白和内吞陷的 I 型肌球蛋白相互作用,作为细胞器间桥发挥作用。这些蛋白质不仅促进接触部位的局部肌动蛋白组装,而且也是 ER 自噬所必需的。我们提出,局部肌动蛋白聚合可以将 ER 片材的边缘从细胞皮质推向靠近液泡的自噬体组装部位。