The MST1/2-SAV1 complex of the Hippo pathway promotes ciliogenesis.

Nature communications (2014-11-05)
Miju Kim, Minchul Kim, Mi-Sun Lee, Cheol-Hee Kim, Dae-Sik Lim
RESUMEN

Primary cilia are microtubule-based organelles that protrude from polarized epithelial cells. Although many structural and trafficking molecules that regulate ciliogenesis have been discovered, signalling proteins are not well defined. Here we show that the MST1/2-SAV1 complex, a core component of the Hippo pathway, promotes ciliogenesis. MST1 is activated during ciliogenesis and localizes to the basal body of cilia. Depletion of MST1/2 or SAV1 impairs ciliogenesis in cultured cells and induces ciliopathy phenotypes in zebrafish. MST1/2-SAV1 regulates ciliogenesis through two independent mechanisms: MST1/2 binds and phosphorylates Aurora kinase A (AURKA), leading to dissociation of the AURKA/HDAC6 cilia-disassembly complex; and MST1/2-SAV1 associates with the NPHP transition-zone complex, promoting ciliary localization of multiple ciliary cargoes. Our results suggest that components of the Hippo pathway contribute to establish a polarized cell structure in addition to regulating proliferation.

MATERIALES
Referencia del producto
Marca
Descripción del producto

Sigma-Aldrich
Monoclonal Anti-β-Actin antibody produced in mouse, clone AC-74, ascites fluid
Sigma-Aldrich
Monoclonal Anti-Acetylated Tubulin antibody produced in mouse, clone 6-11B-1, purified from hybridoma cell culture
Sigma-Aldrich
Anti-γ-Tubulin antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution

Redes sociales

LinkedIn icon
Twitter icon
Facebook Icon
Instagram Icon

Merck

Investigación. Desarrollo. Producción.

Somos un proveedor líder para la industria de Ciencias de la Vida con soluciones y servicios para investigación, desarrollo y producción biotecnológicos, y para desarrollo y producción de tratamientos farmacéuticos

© 2021 Merck KGaA, Darmstadt, Alemania y/o sus filiales. Todos los derechos reservados.

Queda estrictamente prohibida la reproducción sin permiso de cualquiera de los materiales de la página web.