Autophagy ensures the turnover of cytoplasm and requires the coordinated action of Atg proteins, some of which also have moonlighting functions in higher eukaryotes. Here we show that the transmembrane protein Atg9 is required for female fertility, and its loss leads to defects in actin cytoskeleton organization in the ovary and enhances filopodia formation in neurons in Drosophila. Atg9 localizes to the plasma membrane anchor points of actin cables and is also important for the integrity of the cortical actin network. Of note, such phenotypes are not seen in other Atg mutants, suggesting that these are independent of autophagy defects. Mechanistically, we identify the known actin regulators profilin and Ena/VASP as novel binding partners of Atg9 based on microscopy, biochemical, and genetic interactions. Accordingly, the localization of both profilin and Ena depends on Atg9. Taken together, our data identify a new and unexpected role for Atg9 in actin cytoskeleton regulation.

中文翻译：

---

果蝇Atg9通过与profilin和Ena的相互作用来调节肌动蛋白的细胞骨架。

自噬可确保细胞质的周转并需要Atg蛋白的协同作用，其中一些在高级真核生物中也具有月光作用。在这里，我们显示女性生殖力需要跨膜蛋白Atg9，其丢失导致卵巢肌动蛋白细胞骨架组织的缺陷，并增强果蝇神经元的丝状伪足形成。Atg9定位于肌动蛋白电缆的质膜锚定点，对于皮质肌动蛋白网络的完整性也很重要。值得注意的是，在其他Atg突变体中未见到此类表型，表明这些表型与自噬缺陷无关。从机理上讲，我们基于显微镜，生化和遗传相互作用将已知的肌动蛋白调节剂profilin和Ena / VASP确定为Atg9的新型结合伴侣。因此，profilin和Ena的定位均取决于Atg9。综上所述，我们的数据确定了Atg9在肌动蛋白细胞骨架调控中的新的和意想不到的作用。