Boundary cells restrict dystroglycan trafficking to control basement membrane sliding during tissue remodeling

eLife

Eric L Hastie¹  Lin Wang²  David R Sherwood³  Lara M Linden³  Zheng Wang⁴  Qiuyi Chi⁴  Alan Chen⁵  Wanqing Shen⁵  Shelly TH McClatchey⁵ 

[1] Department of Gastrointestinal Surgery, Union Hospital, Wuhan, China;Development and Molecular Oncology Laboratory, Union Hospital, Wuhan, China;Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;Center for Tissue Engineering and Regenerative Medicine, Union Hospital, Wuhan, China;Department of Biology, Duke University, Durham, United States;

关键词: basement membrane;    morphogenesis;    Notch signaling;    Sec14 family phospholipid transfer protein;    dystroglycan;    membrane transport;   

DOI  :  10.7554/eLife.17218

来源: DOAJ

【 摘 要 】

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 in C. 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 of ctg-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.

【 授权许可】

Unknown