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

Pettitt J, Cox EA, Broadbent ID, Flett A, Hardin J - J. Cell Biol. (2003)

Bottom Line: We have examined the role of the single Caenorhabditis elegans p120ctn homologue JAC-1 (juxtamembrane domain [JMD]-associated catenin) during epidermal morphogenesis.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Cell Biology, University of Aberdeen Institute of Medical Sciences, Aberdeen AB25 2ZD, Scotland, UK. j.pettitt@abdn.ac.uk

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/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.

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JAC-1–GFP localizes to adherens junctions in an HMR-1–dependent manner. (A–C) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for HMR-1 (red). The merged image is shown in C, and the boxed region is enlarged 2.5× in C'. (D–F) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for AJM-1 (red). The merged image is shown in F, and the boxed region is enlarged 2.5× in F'. (G and H) JAC-1–GFP expression in a wild-type (G) and hmr-1(zu389) embryo (H) of approximately the same age. Bar, 10 μm.
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fig3: JAC-1–GFP localizes to adherens junctions in an HMR-1–dependent manner. (A–C) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for HMR-1 (red). The merged image is shown in C, and the boxed region is enlarged 2.5× in C'. (D–F) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for AJM-1 (red). The merged image is shown in F, and the boxed region is enlarged 2.5× in F'. (G and H) JAC-1–GFP expression in a wild-type (G) and hmr-1(zu389) embryo (H) of approximately the same age. Bar, 10 μm.

Mentions: To determine if JAC-1 localizes specifically to adherens junctions, embryos expressing JAC-1–GFP were stained for HMR-1. We found that JAC-1–GFP and HMR-1 precisely colocalize in the epidermis (Fig. 3Figure 3.


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

Pettitt J, Cox EA, Broadbent ID, Flett A, Hardin J - J. Cell Biol. (2003)

JAC-1–GFP localizes to adherens junctions in an HMR-1–dependent manner. (A–C) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for HMR-1 (red). The merged image is shown in C, and the boxed region is enlarged 2.5× in C'. (D–F) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for AJM-1 (red). The merged image is shown in F, and the boxed region is enlarged 2.5× in F'. (G and H) JAC-1–GFP expression in a wild-type (G) and hmr-1(zu389) embryo (H) of approximately the same age. Bar, 10 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2172718&req=5

fig3: JAC-1–GFP localizes to adherens junctions in an HMR-1–dependent manner. (A–C) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for HMR-1 (red). The merged image is shown in C, and the boxed region is enlarged 2.5× in C'. (D–F) Confocal images showing a lateral view of an embryo expressing JAC-1–GFP (green) stained for AJM-1 (red). The merged image is shown in F, and the boxed region is enlarged 2.5× in F'. (G and H) JAC-1–GFP expression in a wild-type (G) and hmr-1(zu389) embryo (H) of approximately the same age. Bar, 10 μm.
Mentions: To determine if JAC-1 localizes specifically to adherens junctions, embryos expressing JAC-1–GFP were stained for HMR-1. We found that JAC-1–GFP and HMR-1 precisely colocalize in the epidermis (Fig. 3Figure 3.

Bottom Line: We have examined the role of the single Caenorhabditis elegans p120ctn homologue JAC-1 (juxtamembrane domain [JMD]-associated catenin) during epidermal morphogenesis.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Cell Biology, University of Aberdeen Institute of Medical Sciences, Aberdeen AB25 2ZD, Scotland, UK. j.pettitt@abdn.ac.uk

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/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.

Show MeSH
Related in: MedlinePlus