Boundary cells restrict dystroglycan trafficking to control basement membrane sliding during tissue remodeling
- Duke University, United States
- Huazhong University of Science and Technology, China
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 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 and 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.
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Funding
National Institute of General Medical Sciences (GM079320)
- David R Sherwood
National Institute of General Medical Sciences (GM100083)
- David R Sherwood
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2016, McClatchey et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Boundary cells restrict dystroglycan trafficking to control basement membrane sliding during tissue remodeling
eLife 5:e17218.
https://doi.org/10.7554/eLife.17218
