The Invading Anchor Cell Induces Lateral Membrane Constriction during Vulval Lumen Morphogenesis in C. elegans

Publication date: 7 August 2017
Source:Developmental Cell, Volume 42, Issue 3
Author(s): Qiutan Yang, Daniel Roiz, Louisa Mereu, Michael Daube, Alex Hajnal
During epithelial tube morphogenesis, linear arrays of cells are converted into tubular structures through actomyosin-generated intracellular forces that induce tissue invagination and lumen formation. We have investigated lumen morphogenesis in the C. elegans vulva. The first discernible event initiating lumen formation is the apical constriction of the two innermost primary cells (VulF). The VulF cells thereafter constrict their lateral membranes along the apicobasal axis to extend the lumen dorsally. Lateral, but not apical, VulF constriction requires the prior invasion of the anchor cell (AC). The invading AC extends actin-rich protrusions toward VulF, resulting in the formation of a direct AC-VulF interface. The recruitment of the F-BAR-domain protein TOCA-1 to the AC-VulF interface induces the accumulation of force-generating actomyosin, causing a switch from apical to lateral membrane constriction and the dorsal extension of the lumen. Invasive cells may induce shape changes in adjacent cells to penetrate their target tissues.

Teaser

Actomyosin-based forces change cell shapes to sculpt tissues. Using the C. elegans vulva as a model for tube morphogenesis, Yang et al. show that anchor cell invasion of the vulval epithelium reorganizes the actomyosin network and induces lateral membrane constriction through recruitment of F-BAR-domain proteins and activation of CDC-42.


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