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Phosphatidylinositol 3-phosphate (PI3P) is mainly formed via phosphorylation of phosphatidylinositol by class Ⅲ phosphatidylinositol 3-kinase (PI3K-Ⅲ).This lipid regulates several types of endosome dynamics, including fusion, motility and involution.The various effects of PI3P in the endocytic pathway are mostly mediated by cytosolic FYVE-or PX-domain-containing proteins that are recruited to endosome membranes in a tightly regulated fashion.These effectors comprise highly disparate proteins such as kinases, phosphatases, motor proteins and tethers.In addition to these typical PI3P effectors, we have recently identified a novel role for a PI3P effector, namely in formation of interorganellar contact sites.Endosomes and the endoplasmic reticulum (ER), the major organelles of the endocytic and biosynthetic pathways, respectively, have previously not been thought to communicate between each other.However, several recent reports have shown the existence of abundant ER-endosome contact sites that potentially play a role in ER dynamics as well as endosome positioning and maturation.In addition, ER-endosome contact sites have been found to mediate loading of the minus-end-directed microtubule motor dynein onto late endosomes.We have now identified another type of PI3P-dependent ER-endosome contact site that functions in loading of plus-end-directed kinesin molecules onto late endosomes.This results in translocation of late endosomes to the plasma membrane along microtubules and controls protrusion outgrowth and autophagy.Thus,ER-endosome contact sites function as platforms for endosomal loading of kinesin-1 motors that indirectly control autophagy.