RRC ID 83971
Author Martin CG, Bent JS, Hill T, Topalidou I, Singhvi A.
Title Epithelial UNC-23 limits mechanical stress to maintain glia-neuron architecture in C. elegans.
Journal Dev Cell
Abstract For an organ to maintain correct architecture and function, its diverse cellular components must coordinate their size and shape. Although cell-intrinsic mechanisms driving homotypic cell-cell coordination are known, it is unclear how cell shape is regulated across heterotypic cells. We find that epithelial cells maintain the shape of neighboring sense-organ glia-neuron units in adult Caenorhabditis elegans (C. elegans). Hsp co-chaperone UNC-23/BAG2 prevents epithelial cell shape from deforming, and its loss causes head epithelia to stretch aberrantly during animal movement. In the sense-organ glia, amphid sheath (AMsh), this causes progressive fibroblast growth factor receptor (FGFR)-dependent disruption of the glial apical cytoskeleton. Resultant glial cell shape alteration causes concomitant shape change in glia-associated neuron endings. Epithelial UNC-23 maintenance of glia-neuron shape is specific both spatially, within a defined anatomical zone, and temporally, in a developmentally critical period. As all molecular components uncovered are broadly conserved across central and peripheral nervous systems, we posit that epithelia may similarly regulate glia-neuron architecture cross-species.
Volume 59(13)
Pages 1668-1688.e7
Published 2024-7-8
DOI 10.1016/j.devcel.2024.04.005
PII S1534-5807(24)00230-2
PMID 38670103
PMC PMC11233253
MeSH Animals Caenorhabditis elegans* / metabolism Caenorhabditis elegans Proteins* / genetics Caenorhabditis elegans Proteins* / metabolism Cell Shape Cytoskeleton / metabolism Epithelial Cells / cytology Epithelial Cells / metabolism Neuroglia* / metabolism Neurons* / metabolism Receptors, Fibroblast Growth Factor / genetics Receptors, Fibroblast Growth Factor / metabolism Stress, Mechanical
Resource
C.elegans tm2318 tm832 tm544