The Caenorhabditis elegans p120 catenin homologue, JAC-1, modulates cadherin–catenin function during epidermal morphogenesis

Abstract

The cadherin–catenin complex is essential for tissue morphogenesis during animal development. In cultured mammalian cells, p120 catenin (p120ctn) is an important regulator of cadherin–catenin complex function. However, information on the role of p120ctn family members in cadherin-dependent events in vivo is limited. We have examined the role of the single Caenorhabditis elegans p120ctn homologue JAC-1 (juxtamembrane domain [JMD]–associated catenin) during epidermal morphogenesis. Similar to other p120ctn family members, JAC-1 binds the JMD of the classical cadherin HMR-1, and GFP-tagged JAC-1 localizes to adherens junctions in an HMR-1–dependent manner. Surprisingly, depleting JAC-1 expression using RNA interference (RNAi) does not result in any obvious defects in embryonic or postembryonic development. However, jac-1(RNAi) does increase the severity and penetrance of morphogenetic defects caused by a hypomorphic mutation in the hmp-1/α-catenin gene. In these hmp-1 mutants, jac-1 depletion causes failure of the embryo to elongate into a worm-like shape, a process that involves contraction of the epidermis. Associated with failed elongation is the detachment of actin bundles from epidermal adherens junctions and failure to maintain cadherin in adherens junctions. These results suggest that JAC-1 acts as a positive modulator of cadherin function in C. elegans.

Involvement of p120 Carboxy-Terminal Domain in Cadherin Trafficking

“…Davis et al (Davis et al, 2003) also discussed that murine p120KO is embryonic lethal. On the other hand, experiments in C. elegans and Drosophila indicated that p120 is not essential in these organisms (Myster et al, 2003;Pettitt et al, 2003). Moreover, recent reports indicated that conditional KO of p120 in mouse epidermis and salivary gland caused severe defects in inflammatory response and cell differentiation, respectively, but not cellular lethality Perez-Moreno et al, 2006).…”

Anchoring Junctions As Drug Targets: Role in Contraceptive Development

“…It is noteworthy that only cadherins can target p120 catenin to the plasma membrane (Thoreson et al, 2000), and membrane localization of p120 catenin is sufficient to induce its phosphorylation (Xia et al, 2006b). Deletion of p120 catenin in Caenorhabditis elegans resulted in germline cytokinesis defects and sterility (Pettitt et al, 2003;Skop et al, 2004), whereas a loss-of-function study in D. melanogaster, which only contain p120 catenin and not other members of this protein family, showed that p120 catenin is not an essential component of the adherens junction (Myster et al, 2003). As discussed above, this is in sharp contrast to studies in mammals, which suggest that p120 is indispensable for adhesive function.…”

Adherens Junctions in Myelinating Schwann Cells Stabilize Schmidt-Lanterman Incisures via Recruitment of p120 Catenin to E-Cadherin

“…p120 catenin (p120ctn), which binds to the E-cadherin juxtamembrane domain (JMD), can regulate cadherin-mediated adhesion (Aono et al, 1999;Thoreson et al, 2000) by a mechanism that appears to involve cadherin transport and stabilization at the membrane (Ireton et al, 2002;Chen et al, 2003;Davis et al, 2003;Xiao et al, 2003). Surprisingly, the p120ctn gene is not required for invertebrate development (Myster et al, 2003;Pettitt et al, 2003), but recent studies using a depletion-rescue strategy in Xenopus indicate an essential role for p120ctn in early development possibly through an interplay with Rho GTPases (Fang et al, 2004).…”