Synergistic effects of hmp-2/β-catenin and sma-1/βH-spectrin on epidermal morphogenesis in Caenorhabditis elegans

During embryonic development, changes to cell shape, structure, and location act together to construct an organism’s overall form. Epidermal morphogenesis in Caenorhabditis elegans has been a well-studied model for these types of events as this epithelial tissue has substructures like cell-cell and cell-matrix adhesions similar to those in vertebrates (Hsiao and Chisholm 2012). Epidermal cells arise on the dorsal surface of the C. elegans embryo with different subsets of cells undergoing various morphogenetic changes to wrap the embryo in an epithelial sheet (Chisholm and Hardin 2005). During dorsal intercalation, two rows of epithelial cells interdigitate with one another to become a single row along the anterior-posterior axis (Priess and Hirsh 1986; Williams-Masson et al. 1998). Additional cells from either side of the embryo migrate towards the ventral midline, forming new cell-cell adhesions with their contralateral neighbors (Priess and Hirsh 1986; Williams-Masson et al. 1997; Costa et al. 1998). Contractions along circumferential F-actin bundles in the epidermis then change the shape of the cells to drive elongation of the animal along the anterior-posterior axis (Priess and Hirsh 1986). The spectrin cytoskeleton lies apically between the plasma membrane and circumferential F-actin bundles and is thought to be important in structurally supporting the F-actin network during these contractions (Praitis et al. 2005; Lardennois et al. 2019). Homozygous mutant animals of sma-1(ru18), a putative null allele of sma-1/βH-spectrin, are shorter than wildtype with severe disruptions in F-actin bundles normally located at the apical surface (McKeown et al. 1998; Praitis et al. 2005). Since F-actin bundles are also anchored to cadherin-based adhesions at dorsal-ventral cell boundaries, disruption of HMR-1/cadherin, HMP-2/β-catenin, or HMP-1/α-catenin also results in elongation defects and a loss of F-actin at adherens junctions, as well as embryonic lethality (Costa et al. 1998).