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Published 7 July 2003. doi:10.1083/jcb.200212136
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© The Rockefeller University Press, 0021-9525/2003/7/15 $5.00
The Journal of Cell Biology, Volume 162, Number 1, 15-22

Report

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



Jonathan Pettitt1, Elisabeth A. Cox2, Ian D. Broadbent1, Aileen Flett1 and Jeff Hardin2

1 Department of Molecular and Cell Biology, University of Aberdeen Institute of Medical Sciences, Aberdeen AB25 2ZD, UK
2 Department of Zoology, University of Wisconsin, Madison, WI 53706

Address correspondence to Jonathan Pettitt, Department of Molecular and Cell Biology, University of Aberdeen Institute of Medical Sciences, Aberdeen AB25 2ZD, UK. Tel.: 44-1224-273037. Fax: 44-1224-273144. E-mail: j.pettitt{at}abdn.ac.uk

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/{alpha}-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.

Key Words: adherens junctions; p120ctn; {alpha}-catenin; embryo development; actin filaments

J. Pettitt and E.A. Cox contributed equally to this work.

The online version of this article includes supplemental material.

* Abbreviations used in this paper: Armadillo, Arm; CFB, circumferential actin filament bundle; Fn3, fibronectin type III; JMD, juxtamembrane domain; p120 catenin, p120ctn; RNAi, RNA interference.


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