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Drosophila p120catenin plays a supporting role in cell adhesion but is not an essential adherens junction component.

Myster SH, Cavallo R, Anderson CT, Fox DT, Peifer M - J. Cell Biol. (2003)

Bottom Line: We generated alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function.However, p120 mutations strongly enhance mutations in the genes encoding DE-cadherin or Armadillo, the beta-catenin homologue.Finally, we examined the localization of p120 during embryogenesis. p120 localizes to adherens junctions, but its localization there is less universal than that of core adherens junction proteins.

View Article: PubMed Central - PubMed

Affiliation: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

ABSTRACT
Cadherin-catenin complexes, localized to adherens junctions, are essential for cell-cell adhesion. One means of regulating adhesion is through the juxtamembrane domain of the cadherin cytoplasmic tail. This region is the binding site for p120, leading to the hypothesis that p120 is a key regulator of cell adhesion. p120 has also been suggested to regulate the GTPase Rho and to regulate transcription via its binding partner Kaiso. To test these hypothesized functions, we turned to Drosophila, which has only a single p120 family member. It localizes to adherens junctions and binds the juxtamembrane region of DE-cadherin (DE-cad). We generated alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function. However, p120 mutations strongly enhance mutations in the genes encoding DE-cadherin or Armadillo, the beta-catenin homologue. Finally, we examined the localization of p120 during embryogenesis. p120 localizes to adherens junctions, but its localization there is less universal than that of core adherens junction proteins. Together, these data suggest that p120 is an important positive modulator of adhesion but that it is not an essential core component of adherens junctions.

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p120 mRNA is ubiquitously expressed but enriched in certain tissues. Embryos at indicated stages, probed by situ hybridization for expression of p120 mRNA (A–D and F) or with a sense strand p120 control probe (E). Anterior is to the left and dorsal is up. In B, white arrows indicate the neurectoderm and mesoderm of the germband. Certain tissues accumulate elevated levels of p120 mRNA, e.g., the posterior midgut (B, black arrow), brain and CNS (C and F, white arrows), migrating anterior and posterior midgut (C, black arrows), cells forming the midgut constriction (D, arrow). (F) Stage 14 wild-type and mutant homozygous for a deletion removing p120 (Df[2R]M41A8), showing remaining maternal mRNA.
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fig7: p120 mRNA is ubiquitously expressed but enriched in certain tissues. Embryos at indicated stages, probed by situ hybridization for expression of p120 mRNA (A–D and F) or with a sense strand p120 control probe (E). Anterior is to the left and dorsal is up. In B, white arrows indicate the neurectoderm and mesoderm of the germband. Certain tissues accumulate elevated levels of p120 mRNA, e.g., the posterior midgut (B, black arrow), brain and CNS (C and F, white arrows), migrating anterior and posterior midgut (C, black arrows), cells forming the midgut constriction (D, arrow). (F) Stage 14 wild-type and mutant homozygous for a deletion removing p120 (Df[2R]M41A8), showing remaining maternal mRNA.

Mentions: Together these data suggest that p120 is not an essential core component of AJs but instead is a modulator that plays a critical role when cadherin–catenin function is compromised. Thus, one might hypothesize that although p120 would localize to AJs, its level there might vary depending on the situation. Embryogenesis provides a superb place to address this, since one can examine cells facing diverse cell biological challenges. We first examined the expression of p120 mRNA (Fig. 7). It is maternally contributed, and maternal mRNA persists to late stages, since it can be detected in late stage embryos homozygous for a Deficiency removing p120 (Fig. 7 F). When zygotic transcription begins, p120 mRNA is found in all cells (Fig. 7 A). It remains on in all three germ layers during gastrulation (Fig. 7 B, arrows), and expression continues in all or virtually all tissues throughout embryogenesis (Fig. 7, C, D, and F). However, there is elevated expression in certain tissues, many of which are undergoing morphogenetic movements. These include the invaginating posterior midgut (Fig. 7 B, black arrow), the central nervous system (CNS) (Fig. 7, C and F, white arrows), the migrating anterior and posterior midguts (Fig. 7 C, black arrows), the foregut and hindgut, and cells forming the midgut constrictions (Fig. 7 D, arrow).


Drosophila p120catenin plays a supporting role in cell adhesion but is not an essential adherens junction component.

Myster SH, Cavallo R, Anderson CT, Fox DT, Peifer M - J. Cell Biol. (2003)

p120 mRNA is ubiquitously expressed but enriched in certain tissues. Embryos at indicated stages, probed by situ hybridization for expression of p120 mRNA (A–D and F) or with a sense strand p120 control probe (E). Anterior is to the left and dorsal is up. In B, white arrows indicate the neurectoderm and mesoderm of the germband. Certain tissues accumulate elevated levels of p120 mRNA, e.g., the posterior midgut (B, black arrow), brain and CNS (C and F, white arrows), migrating anterior and posterior midgut (C, black arrows), cells forming the midgut constriction (D, arrow). (F) Stage 14 wild-type and mutant homozygous for a deletion removing p120 (Df[2R]M41A8), showing remaining maternal mRNA.
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fig7: p120 mRNA is ubiquitously expressed but enriched in certain tissues. Embryos at indicated stages, probed by situ hybridization for expression of p120 mRNA (A–D and F) or with a sense strand p120 control probe (E). Anterior is to the left and dorsal is up. In B, white arrows indicate the neurectoderm and mesoderm of the germband. Certain tissues accumulate elevated levels of p120 mRNA, e.g., the posterior midgut (B, black arrow), brain and CNS (C and F, white arrows), migrating anterior and posterior midgut (C, black arrows), cells forming the midgut constriction (D, arrow). (F) Stage 14 wild-type and mutant homozygous for a deletion removing p120 (Df[2R]M41A8), showing remaining maternal mRNA.
Mentions: Together these data suggest that p120 is not an essential core component of AJs but instead is a modulator that plays a critical role when cadherin–catenin function is compromised. Thus, one might hypothesize that although p120 would localize to AJs, its level there might vary depending on the situation. Embryogenesis provides a superb place to address this, since one can examine cells facing diverse cell biological challenges. We first examined the expression of p120 mRNA (Fig. 7). It is maternally contributed, and maternal mRNA persists to late stages, since it can be detected in late stage embryos homozygous for a Deficiency removing p120 (Fig. 7 F). When zygotic transcription begins, p120 mRNA is found in all cells (Fig. 7 A). It remains on in all three germ layers during gastrulation (Fig. 7 B, arrows), and expression continues in all or virtually all tissues throughout embryogenesis (Fig. 7, C, D, and F). However, there is elevated expression in certain tissues, many of which are undergoing morphogenetic movements. These include the invaginating posterior midgut (Fig. 7 B, black arrow), the central nervous system (CNS) (Fig. 7, C and F, white arrows), the migrating anterior and posterior midguts (Fig. 7 C, black arrows), the foregut and hindgut, and cells forming the midgut constrictions (Fig. 7 D, arrow).

Bottom Line: We generated alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function.However, p120 mutations strongly enhance mutations in the genes encoding DE-cadherin or Armadillo, the beta-catenin homologue.Finally, we examined the localization of p120 during embryogenesis. p120 localizes to adherens junctions, but its localization there is less universal than that of core adherens junction proteins.

View Article: PubMed Central - PubMed

Affiliation: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

ABSTRACT
Cadherin-catenin complexes, localized to adherens junctions, are essential for cell-cell adhesion. One means of regulating adhesion is through the juxtamembrane domain of the cadherin cytoplasmic tail. This region is the binding site for p120, leading to the hypothesis that p120 is a key regulator of cell adhesion. p120 has also been suggested to regulate the GTPase Rho and to regulate transcription via its binding partner Kaiso. To test these hypothesized functions, we turned to Drosophila, which has only a single p120 family member. It localizes to adherens junctions and binds the juxtamembrane region of DE-cadherin (DE-cad). We generated alleles of p120 and found that mutants are viable and fertile and have no substantial changes in junction structure or function. However, p120 mutations strongly enhance mutations in the genes encoding DE-cadherin or Armadillo, the beta-catenin homologue. Finally, we examined the localization of p120 during embryogenesis. p120 localizes to adherens junctions, but its localization there is less universal than that of core adherens junction proteins. Together, these data suggest that p120 is an important positive modulator of adhesion but that it is not an essential core component of adherens junctions.

Show MeSH
Related in: MedlinePlus