@article{a98305289d6f48de8e1b6e6af71987cd,
title = "The Tricellular Junction Protein Sidekick Regulates Vertex Dynamics to Promote Bicellular Junction Extension",
abstract = "Remodeling of cell-cell junctions drives cell intercalation that causes tissue movement during morphogenesis through the shortening and growth of bicellular junctions. The growth of new junctions is essential for continuing and then completing cellular dynamics and tissue shape sculpting; however, the mechanism underlying junction growth remains obscure. We investigated Drosophila genitalia rotation where continuous cell intercalation occurs to show that myosin II accumulating at the vertices of a new junction is required for the junction growth. This myosin II accumulation requires the adhesive transmembrane protein Sidekick (Sdk), which localizes to the adherens junctions (AJs) of tricellular contacts (tAJs). Sdk also localizes to and blocks the accumulation of E-Cadherin at newly formed growing junctions, which maintains the growth rate. We propose that Sdk facilitates tAJ movement by mediating myosin II-driven contraction and altering the adhesive properties at the tAJs, leading to cell-cell junction extension during persistent junction remodeling.",
keywords = "CALI, collective cell movement, Drosophila, epithelial cells, junction remodeling, sidekick, tricellular junction",
author = "Hiroyuki Uechi and Erina Kuranaga",
note = "Funding Information: We thank V. Auld for providing the anti-Gliotactin antibodies; J.E. Treisman for providing the pUAST-HA-sdk plasmid; H. Oda for providing the pCaspR-Ubi-E-Cad-GFP plasmid; F. Matsuzaki and S. Yoshiura for providing the S2 cells; D. Umetsu for helping to generate the MRLC::SuperNova knockin fly; A. Isomura, Y. Umegaki, S. Sato, K. Takahashi, and A. Kuranaga for supporting the experiments; T. Lecuit, S. Hayashi, and Y. Ogura for their critical advice; and all members of our laboratory for discussion. We thank Y. Sato of Carl Zeiss co., Ltd. for technical assistance. We are grateful to L.A. Miglietta and “Clarity editing” for language and technical proofreading of the manuscript. This work was supported by grants from JST CREST grant number JPMJCR1852 , Japan (E.K.); the research grant for Astellas Foundation for Research on Metabolic Disorders (E.K.); the Takeda Science Foundation (E.K.); the Japan Foundation for Applied Enzymology (E.K.); MEXT KAKENHI grant number JP26114003 (E.K.); and JSPS KAKENHI grant numbers JP24687027 (E.K.), JP16H04800 (E.K.), and JP18K14691 (H.U). Publisher Copyright: {\textcopyright} 2019 Elsevier Inc.",
year = "2019",
month = aug,
day = "5",
doi = "10.1016/j.devcel.2019.06.017",
language = "English",
volume = "50",
pages = "327--338.e5",
journal = "Developmental Cell",
issn = "1534-5807",
publisher = "Cell Press",
number = "3",
}