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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • McClatchey, ST; Wang, Z; Linden, LM; Hastie, EL; Wang, L; Shen, W; Chen, A; Chi, Q; Sherwood, DR

Published Date

  • September 23, 2016

Published In

Volume / Issue

  • 5 /

PubMed ID

  • 27661254

Pubmed Central ID

  • 27661254

Electronic International Standard Serial Number (EISSN)

  • 2050-084X

International Standard Serial Number (ISSN)

  • 2050-084X

Digital Object Identifier (DOI)

  • 10.7554/eLife.17218

Language

  • eng