GEI-16 : a novel component of the C. elegans fibrous organelle

Abstract

Animal tissues are maintained by the correct cell-cell contacts and cellular shape. Cell shape and associations are governed by the combined action of the filament cytoskeleton in association with adhesion complexes. Desmosomes and hemidesmosomes are one such class of adhesion complex. From worms to humans epithelial tissues are flattened and made resistant to mechanical stress by desmosomes and hemidesmosomes. These membrane-associated junction complexes are attached to the intermediate filaments (IFs), the strongest and most elastic of the cytoskeletal filaments. In Caenorhabditis elegans, a requirement for the hemidesmosomes first becomes apparent in embryonic morphogenesis. Without functioning hemidesmosomes elongation arrests at the two-fold stage and the embryo never attains its vermiform shape (four-fold elongation). Characterisation of the loss of larva-specific intermediate filaments has shown that functional hemidesmosomes are necessary for tissue integrity and the continued development of the worm at all stages. It appears that, as in other animals, hemidesmosomes maintain a squamified epithelium which resists and equalises shearing forces generated during morphogenetic and locomotive movement. This thesis discusses the discovery of GEI-16 (PAT-12), a new component of the hemidesmosome and fibrous organelle (FO) in C. elegans. Discovered in a screen for uncharacterised, pan-nematode genes with vital functions, GEI-16 is necessary for all life stages. Loss of gei-16 leads to paralysis, muscle detachment and developmental arrest during the elongation step of embryogenesis. The same phenotype occurs in all stages of development if gei-16 is lacking. GEI-16 is likely to function with VAB-10 and the actin cytoskeleton to organise and strengthen the fibrous organelle during elongation. Show more