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We previously demonstrated that efficient<jats:italic>C. parvum<\/jats:italic>invasion of biliary epithelial cells (cholangiocytes) requires host cell actin polymerization and localized membrane translocation\/insertion of Na<jats:sup>+<\/jats:sup>\/glucose cotransporter 1 (SGLT1) and of aquaporin 1 (Aqp1), a water channel, at the attachment site. The resultant localized water influx facilitates parasite cellular invasion by promoting host-cell membrane protrusion. However, the molecular mechanisms by which<jats:italic>C. parvum<\/jats:italic>induces membrane translocation\/insertion of SGLT1\/Aqp1 are obscure. We report here that cultured human cholangiocytes express several nonmuscle myosins, including myosins IIA and IIB. Moreover,<jats:italic>C. parvum<\/jats:italic>infection of cultured cholangiocytes results in the localized selective aggregation of myosin IIB but not myosin IIA at the region of parasite attachment, as assessed by dual-label immunofluorescence confocal microscopy. Concordantly, treatment of cells with the myosin light chain kinase inhibitor ML-7 or the myosin II-specific inhibitor blebbistatin or selective RNA-mediated repression of myosin IIB significantly inhibits (<jats:italic>P<\/jats:italic>&lt; 0.05)<jats:italic>C. parvum<\/jats:italic>cellular invasion (by 60 to 80%). Furthermore ML-7 and blebbistatin significantly decrease (<jats:italic>P<\/jats:italic>&lt; 0.02)<jats:italic>C. parvum<\/jats:italic>-induced accumulation of SGLT1 at infection sites (by approximately 80%). Thus, localized actomyosin-dependent membrane translocation of transporters\/channels initiated by<jats:italic>C. parvum<\/jats:italic>is essential for membrane extension and parasite internalization, a phenomenon that may also be relevant to the mechanisms of cell membrane protrusion in general.<\/jats:p>","DOI":"10.1128\/iai.00077-10","type":"journal-article","created":{"date-parts":[[2010,5,11]],"date-time":"2010-05-11T03:49:07Z","timestamp":1273549747000},"page":"2927-2936","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":10,"title":["Cholangiocyte Myosin IIB Is Required for Localized Aggregation of Sodium Glucose Cotransporter 1 to Sites of<i>Cryptosporidium parvum<\/i>Cellular Invasion and Facilitates Parasite Internalization"],"prefix":"10.1128","volume":"78","author":[{"given":"Steven P.","family":"O'Hara","sequence":"first","affiliation":[{"name":"Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, and Mayo Clinic Center for Cell Signaling, Mayo Clinic, Rochester, Minnesota 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gabriella B.","family":"Gajdos","sequence":"additional","affiliation":[{"name":"Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, and Mayo Clinic Center for Cell Signaling, Mayo Clinic, Rochester, Minnesota 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christy E.","family":"Trussoni","sequence":"additional","affiliation":[{"name":"Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, and Mayo Clinic Center for Cell Signaling, Mayo Clinic, Rochester, Minnesota 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrick L.","family":"Splinter","sequence":"additional","affiliation":[{"name":"Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, and Mayo Clinic Center for Cell Signaling, Mayo Clinic, Rochester, Minnesota 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicholas F.","family":"LaRusso","sequence":"additional","affiliation":[{"name":"Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, and Mayo Clinic Center for Cell Signaling, Mayo Clinic, Rochester, Minnesota 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2002.020818"},{"key":"e_1_3_2_3_2","first-page":"82S","volume":"38","year":"1991","unstructured":"Aji, T., T. 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