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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 cooperates with HMP-1 to promote the anchorage of CFBs and the maintenance of HMR-1 distribution during elongation of the embryonic epidermis. (A) Images showing representative embryos stained for actin (a–d) or HMR-1 (e–h). (a and e) Wild-type embryos. (b and f) jac-1(RNAi) embryos. (c and g) hmp-1(fe4) embryos. (d and h) hmp-1(fe4); jac-1(RNAi) embryos. In c, the arrow points to an abnormally thick actin filament bundle. In g, the arrow indicates an area with no HMR-1 staining, and the arrowhead indicates an area of punctate HMR-1 staining. All images are lateral views with the dorsal side up. Bar, 10 μm. (B) An epidermal seam cell from an hmp-1(fe4); jac-1(RNAi) embryo double labeled for HMR-1 and actin. Bar, 5 μm.
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fig5: JAC-1 cooperates with HMP-1 to promote the anchorage of CFBs and the maintenance of HMR-1 distribution during elongation of the embryonic epidermis. (A) Images showing representative embryos stained for actin (a–d) or HMR-1 (e–h). (a and e) Wild-type embryos. (b and f) jac-1(RNAi) embryos. (c and g) hmp-1(fe4) embryos. (d and h) hmp-1(fe4); jac-1(RNAi) embryos. In c, the arrow points to an abnormally thick actin filament bundle. In g, the arrow indicates an area with no HMR-1 staining, and the arrowhead indicates an area of punctate HMR-1 staining. All images are lateral views with the dorsal side up. Bar, 10 μm. (B) An epidermal seam cell from an hmp-1(fe4); jac-1(RNAi) embryo double labeled for HMR-1 and actin. Bar, 5 μm.

Mentions: As elongation defects have been associated with defects in the actin cytoskeleton of the epidermis (for review see Chin-Sang and Chisholm, 2000; Simske and Hardin, 2001), we examined the effects of jac-1(RNAi) on actin structure. In wild-type embryos, the circumferential actin filament bundles (CFBs) that drive elongation are evenly distributed in parallel arrays throughout the epidermis (Fig. 5Figure 5.


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 cooperates with HMP-1 to promote the anchorage of CFBs and the maintenance of HMR-1 distribution during elongation of the embryonic epidermis. (A) Images showing representative embryos stained for actin (a–d) or HMR-1 (e–h). (a and e) Wild-type embryos. (b and f) jac-1(RNAi) embryos. (c and g) hmp-1(fe4) embryos. (d and h) hmp-1(fe4); jac-1(RNAi) embryos. In c, the arrow points to an abnormally thick actin filament bundle. In g, the arrow indicates an area with no HMR-1 staining, and the arrowhead indicates an area of punctate HMR-1 staining. All images are lateral views with the dorsal side up. Bar, 10 μm. (B) An epidermal seam cell from an hmp-1(fe4); jac-1(RNAi) embryo double labeled for HMR-1 and actin. Bar, 5 μm.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2172718&req=5

fig5: JAC-1 cooperates with HMP-1 to promote the anchorage of CFBs and the maintenance of HMR-1 distribution during elongation of the embryonic epidermis. (A) Images showing representative embryos stained for actin (a–d) or HMR-1 (e–h). (a and e) Wild-type embryos. (b and f) jac-1(RNAi) embryos. (c and g) hmp-1(fe4) embryos. (d and h) hmp-1(fe4); jac-1(RNAi) embryos. In c, the arrow points to an abnormally thick actin filament bundle. In g, the arrow indicates an area with no HMR-1 staining, and the arrowhead indicates an area of punctate HMR-1 staining. All images are lateral views with the dorsal side up. Bar, 10 μm. (B) An epidermal seam cell from an hmp-1(fe4); jac-1(RNAi) embryo double labeled for HMR-1 and actin. Bar, 5 μm.
Mentions: As elongation defects have been associated with defects in the actin cytoskeleton of the epidermis (for review see Chin-Sang and Chisholm, 2000; Simske and Hardin, 2001), we examined the effects of jac-1(RNAi) on actin structure. In wild-type embryos, the circumferential actin filament bundles (CFBs) that drive elongation are evenly distributed in parallel arrays throughout the epidermis (Fig. 5Figure 5.

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