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PACSIN2 KO enterocytes exhibit reduced numbers of microvilli and defects in the microvillar ultrastructure, with membranes lifting away from rootlets of core bundles. Dynamin2, a PACSIN2 binding partner, and other endocytic factors were also lost from their normal localization near microvillar rootlets. To determine whether loss of endocytic machinery could explain defects in microvillar morphology, we examined the impact of PACSIN2 KD and endocytosis inhibition on live intestinal epithelial cells. These assays revealed that when endocytic vesicle scission fails, tubules are pulled into the cytoplasm and this, in turn, leads to a membrane-lifting phenomenon reminiscent of that observed at PACSIN2 KO brush borders. These findings lead to a new model where inward forces generated by endocytic machinery on the plasma membrane control the membrane wrapping of cell surface protrusions.<\/jats:p>","DOI":"10.1091\/mbc.e19-06-0352","type":"journal-article","created":{"date-parts":[[2019,8,7]],"date-time":"2019-08-07T12:50:23Z","timestamp":1565182223000},"page":"2515-2526","source":"Crossref","is-referenced-by-count":23,"title":["PACSIN2-dependent apical endocytosis regulates the morphology of epithelial microvilli"],"prefix":"10.1091","volume":"30","author":[{"given":"Meagan M.","family":"Postema","sequence":"first","affiliation":[{"name":"Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, University Medical Center, Nashville, TN 37232"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan E.","family":"Grega-Larson","sequence":"additional","affiliation":[{"name":"Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, 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