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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(RNAi) enhances the elongation defects of hmp-1(fe4) mutants. (A) Agarose gel electrophoresis of semiquantitative RT-PCR reactions derived from worms grown on HT115(DE3) bacteria carrying either the empty RNAi feeding vector or the jac-1(RNAi) feeding vector. Numbers on top indicate the number of amplification cycles. Numbers on the side indicate the base pair size of the marker DNAs. (B) Nomarski images at 30-min intervals of representative embryos undergoing elongation. Corresponding videos (Videos 1–4) are available at http://www.jcb.org/cgi/content/full/jcb.200212136/DC1. (a) Wild-type embryo. (b) jac-1(RNAi) embryo. (c) hmp-1(fe4) embryo. (d) hmp-1(fe4); jac-1(RNAi) embryo. Bar, 10 μm.
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fig4: jac-1(RNAi) enhances the elongation defects of hmp-1(fe4) mutants. (A) Agarose gel electrophoresis of semiquantitative RT-PCR reactions derived from worms grown on HT115(DE3) bacteria carrying either the empty RNAi feeding vector or the jac-1(RNAi) feeding vector. Numbers on top indicate the number of amplification cycles. Numbers on the side indicate the base pair size of the marker DNAs. (B) Nomarski images at 30-min intervals of representative embryos undergoing elongation. Corresponding videos (Videos 1–4) are available at http://www.jcb.org/cgi/content/full/jcb.200212136/DC1. (a) Wild-type embryo. (b) jac-1(RNAi) embryo. (c) hmp-1(fe4) embryo. (d) hmp-1(fe4); jac-1(RNAi) embryo. Bar, 10 μm.

Mentions: As no jac-1 mutants currently exist, the role of JAC-1 during epidermal morphogenesis was assessed through depleting its expression via RNA interference (RNAi). Depletion of jac-1 function in wild-type animals did not produce any observable defects. We also examined the effect of jac-1(RNAi) on a mutant strain (NL2099) shown to be hypersensitive to RNAi (Simmer et al., 2002) and, similarly, did not detect a mutant phenotype. Semiquantitative RT-PCR analysis revealed that jac-1 transcript levels were reduced ∼15-fold (15.56 ± 2.30 SD) compared with controls (Fig. 4Figure 4.


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(RNAi) enhances the elongation defects of hmp-1(fe4) mutants. (A) Agarose gel electrophoresis of semiquantitative RT-PCR reactions derived from worms grown on HT115(DE3) bacteria carrying either the empty RNAi feeding vector or the jac-1(RNAi) feeding vector. Numbers on top indicate the number of amplification cycles. Numbers on the side indicate the base pair size of the marker DNAs. (B) Nomarski images at 30-min intervals of representative embryos undergoing elongation. Corresponding videos (Videos 1–4) are available at http://www.jcb.org/cgi/content/full/jcb.200212136/DC1. (a) Wild-type embryo. (b) jac-1(RNAi) embryo. (c) hmp-1(fe4) embryo. (d) hmp-1(fe4); jac-1(RNAi) embryo. Bar, 10 μm.
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Related In: Results  -  Collection

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fig4: jac-1(RNAi) enhances the elongation defects of hmp-1(fe4) mutants. (A) Agarose gel electrophoresis of semiquantitative RT-PCR reactions derived from worms grown on HT115(DE3) bacteria carrying either the empty RNAi feeding vector or the jac-1(RNAi) feeding vector. Numbers on top indicate the number of amplification cycles. Numbers on the side indicate the base pair size of the marker DNAs. (B) Nomarski images at 30-min intervals of representative embryos undergoing elongation. Corresponding videos (Videos 1–4) are available at http://www.jcb.org/cgi/content/full/jcb.200212136/DC1. (a) Wild-type embryo. (b) jac-1(RNAi) embryo. (c) hmp-1(fe4) embryo. (d) hmp-1(fe4); jac-1(RNAi) embryo. Bar, 10 μm.
Mentions: As no jac-1 mutants currently exist, the role of JAC-1 during epidermal morphogenesis was assessed through depleting its expression via RNA interference (RNAi). Depletion of jac-1 function in wild-type animals did not produce any observable defects. We also examined the effect of jac-1(RNAi) on a mutant strain (NL2099) shown to be hypersensitive to RNAi (Simmer et al., 2002) and, similarly, did not detect a mutant phenotype. Semiquantitative RT-PCR analysis revealed that jac-1 transcript levels were reduced ∼15-fold (15.56 ± 2.30 SD) compared with controls (Fig. 4Figure 4.

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