Cells subjected to stress situations mobilize specific membranes and proteins to initiate autophagy. Phosphatidylinositol-3-phosphate (PI3P), a crucial lipid in membrane dynamics, is known to be essential in this context. In addition to nutriments deprivation, autophagy is also triggered by fluid-flow induced shear stress in epithelial cells, and this specific autophagic response depends on primary cilium (PC) signaling and leads to cell size regulation. Here we report that PI3KC2α, required for ciliogenesis and PC functions, promotes the synthesis of a local pool of PI3P upon shear stress. We show that PI3KC2α depletion in cells subjected to shear stress abolishes ciliogenesis as well as the autophagy and related cell size regulation. We finally show that PI3KC2α and VPS34, the two main enzymes responsible for PI3P synthesis, have different roles during autophagy, depending on the type of cellular stress: while VPS34 is clearly required for starvation-induced autophagy, PI3KC2α participates only in shear stress-dependent autophagy.

中文翻译：

---

PI3P的依赖于PI3KC2α和不依赖VPS34的PI3P生成可响应剪切应力控制主要的纤毛介导的自噬。

处于应激状态的细胞动员特定的膜和蛋白质以启动自噬。在这种情况下，磷脂酰肌醇-3-磷酸酯（PI3P）是膜动力学中的关键脂质，是必不可少的。除营养剥夺外，自噬还由上皮细胞中的液流诱导的切应力触发，这种特定的自噬反应取决于初级纤毛（PC）信号传导并导致细胞大小调节。在这里我们报告纤毛生成和PC功能所需的PI3KC2α促进剪切应力后PI3P局部池的合成。我们表明，PI3KC2α耗竭的细胞受到剪应力消除纤毛发生以及自噬和相关的细胞大小调节。我们最终证明PI3KC2α和VPS34是负责PI3P合成的两种主要酶，