title: Boundary cells restrict dystroglycan trafficking to control basement membrane sliding during tissue remodeling.
abstract: Epithelial cells and their underlying basement membranes (BMs) slide along each other to renew epithelia, shape organs, and enlarge BM openings. How BM sliding is controlled, however, is poorly understood. Using genetic and live cell imaging approaches during uterine-vulval attachment inC. elegans, we have discovered that the invasive uterine anchor cell activates Notch signaling in neighboring uterine cells at the boundary of the BM gap through which it invades to promote BM sliding. Through an RNAi screen, we found that Notch activation upregulates expression ofctg-1, which encodes a Sec14-GOLD protein, a member of the Sec14 phosphatidylinositol-transfer protein superfamily that is implicated in vesicle trafficking. Through photobleaching, targeted knockdown, and cell-specific rescue, our results suggest that CTG-1 restricts BM adhesion receptor DGN-1 (dystroglycan) trafficking to the cell-BM interface, which promotes BM sliding. Together, these studies reveal a new morphogenetic signaling pathway that controls BM sliding to remodel tissues.
authors.affiliation: Department of Biology, Duke University, Durham, United States.
authors.forename: Shelly Th
authors.initials: ST
authors.lastname: McClatchey
authors.affiliation: Center for Tissue Engineering and Regenerative Medicine, Union Hospital, Wuhan, China.|Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.|Department of Gastrointestinal Surgery, Union Hospital, Wuhan, China.|Development and Molecular Oncology Laboratory, Union Hospital, Wuhan, China.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Biology, Duke University, Durham, United States.
authors.forename: Lara M
authors.initials: LM
authors.lastname: Linden
authors.affiliation: Department of Biology, Duke University, Durham, United States.
authors.forename: Eric L
authors.initials: EL
authors.lastname: Hastie
authors.affiliation: Center for Tissue Engineering and Regenerative Medicine, Union Hospital, Wuhan, China.|Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.affiliation: Center for Tissue Engineering and Regenerative Medicine, Union Hospital, Wuhan, China.|Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Wanqing
authors.initials: W
authors.lastname: Shen
authors.affiliation: Department of Biology, Duke University, Durham, United States.
authors.forename: Alan
authors.initials: A
authors.lastname: Chen
authors.affiliation: Department of Biology, Duke University, Durham, United States.
authors.forename: Qiuyi
authors.initials: Q
authors.lastname: Chi
authors.affiliation: Department of Biology, Duke University, Durham, United States.
authors.forename: David R
authors.identifier: 0000-0003-2245-2334
authors.initials: DR
authors.lastname: Sherwood
mesh_terms: D000818:Animals; D001485:Basement Membrane / Q000378:metabolism*; D017173:Caenorhabditis elegans / Q000378:metabolism / Q000502:physiology; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism; D049030:Dystroglycans / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism / Q000502:physiology*; D009068:Movement
chemical_list: D029742:Caenorhabditis elegans Proteins; D049030:Dystroglycans
keywords: C. elegans; Notch signaling; Sec14 family phospholipid transfer protein; basement membrane; cell biology; dystroglycan; membrane transport; morphogenesis