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

• Main Authors: Shelly TH McClatchey, Zheng Wang, Lara M Linden, Eric L Hastie, Lin Wang, Wanqing Shen, Alan Chen, Qiuyi Chi, David R Sherwood
• Format: Article
• Language: English
• Published: eLife Sciences Publications Ltd 2016-09-01
• Series: eLife
• Subjects: basement membrane; morphogenesis; Notch signaling; Sec14 family phospholipid transfer protein; dystroglycan; membrane transport
• Online Access: https://elifesciences.org/articles/17218

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.