Phosphorylation of the Drosophila Adherens Junction Protein Armadillo: Roles for Wingless Signal and Zeste-white 3 Kinase

Peifer, Mark; Pai, Li‐Mei; Casey, Michael J.

doi:10.1006/dbio.1994.1336

Cited by 230 publications

(191 citation statements)

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“…In the absence of Wg, the distribution of Arm was very similar to the distribution of Ecadherin, suggesting that most of the Arm was associated with E-cadherin. As in cl8mEcad cells, expression of E-cadherin led to the accumulation of two forms of Arm, as a result of a difference in phosphorylation on serine and threonine residues, as shown previously (Peifer et al, 1994a).…”

Section: Journal Of Cell Science 119 (12)supporting

confidence: 78%

“…Upon induction of high Ecadherin levels with Cu 2+ , significant amounts of both proteins were also found in the Triton X-100-insoluble pellet fraction (I). al., 1994a;Van Leeuwen et al, 1994). Northern Blot analysis showed that the increase in Arm protein levels was not caused by a change in the steady state levels of Arm mRNA (Fig.…”

Section: Journal Of Cell Science 119 (12)mentioning

confidence: 98%

“…1A). Both the hyperphosphorylated, slower migrating form (henceforth called phosphorylated) and the hypophosphorylated, faster migrating form of Arm (Peifer et al, 1994a) were elevated as a consequence of E-cadherin expression. This is in contrast to the increase in Arm after stimulation with Wg, in which only the hypophosphorylated form of Arm accumulates (Peifer et (cl8mEcad), were analyzed by western blotting with antibodies against mouse E-cadherin, Arm and ␣-catenin.…”

Section: Journal Of Cell Science 119 (12)mentioning

confidence: 99%

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Wingless signaling modulates cadherin-mediated cell adhesion inDrosophilaimaginal disc cells

Wodarz

Stewart

Nelson

et al. 2006

Journal of Cell Science

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Armadillo, the Drosophila homolog of β-catenin, plays a crucial role in both the Wingless signal transduction pathway and cadherin-mediated cell-cell adhesion, raising the possibility that Wg signaling affects cell adhesion. Here, we use a tissue culture system that allows conditional activation of the Wingless signaling pathway and modulation of E-cadherin expression levels. We show that activation of the Wingless signaling pathway leads to the accumulation of hypophosphorylated Armadillo in the cytoplasm and in cellular processes, and to a concomitant reduction of membrane-associated Armadillo. Activation of the Wingless pathway causes a loss of E-cadherin from the cell surface, reduced cell adhesion and increased spreading of the cells on the substratum. After the initial loss of E-cadherin from the cell surface, E-cadherin gene expression is increased by Wingless. We suggest that Wingless signaling causes changes in Armadillo levels and subcellular localization that result in a transient reduction of cadherin-mediated cell adhesion, thus facilitating cell shape changes, division and movement of cells in epithelial tissues.

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Section: Journal Of Cell Science 119 (12)supporting

confidence: 78%

Section: Journal Of Cell Science 119 (12)mentioning

confidence: 98%

Section: Journal Of Cell Science 119 (12)mentioning

confidence: 99%

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Wingless signaling modulates cadherin-mediated cell adhesion inDrosophilaimaginal disc cells

Wodarz

Stewart

Nelson

et al. 2006

Journal of Cell Science

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“…When GSK-3 is inhibited within a protein complex in the Wnt signaling pathway, or by an inhibitor such as lithium, GSK-3 does not phosphorylate b-catenin. The unphosphorylated b-catenin is therefore not degraded, a consequence that leads to increased cellular levels of b-catenin (Behrens et al, 1998;Peifer et al, 1994;Yost et al, 1996). At therapeutically relevant concentrations (serum concentrations between 0.5 and 1.2 mM), lithium increases b-catenin and Wnt-mediated gene expression in the brains of rodents, suggesting relevance to the clinical effects of the drug (De Ferrari et al, 2003;Gould et al, 2004aGould et al, , 2006O'Brien et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

β-Catenin Overexpression in the Mouse Brain Phenocopies Lithium-Sensitive Behaviors

Gould

Einat

O’Donnell

et al. 2007

Neuropsychopharmacol

128

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Lithium inhibits glycogen synthase kinase-3 (GSK-3) at therapeutic concentrations; however, it is unclear if this inhibition and its downstream effects on specific signaling pathways are relevant to the treatment of bipolar disorder and depression. One of the targets of GSK-3 is the transcription factor b-catenin. Normally active GSK-3 phosphorylates b-catenin, leading to its degradation. Inhibition of GSK-3 therefore increases b-catenin. We have utilized transgenic mice to investigate the behavioral consequences of CNS b-catenin overexpression. Transgenic mice overexpressing b-catenin demonstrated behavioral changes similar to those observed following the administration of lithium, including decreased immobility time in the forced swim test (FST). Further, we show that although acute administration of lithium and overexpression of the b-catenin transgene inhibits d-amphetamine-induced hyperlocomotion, neither lithium nor the b-catenin transgene prevents d-amphetamine-induced sensitization, as measured by locomotor activity. Both lithiumtreated and b-catenin mice had an elevated response to d-amphetamine following multiple administrations of the stimulant, though the difference in absolute locomotion was maintained throughout the sensitization time-course. Neither acute lithium nor b-catenin overexpression had an effect on d-amphetamine-induced stereotyped behavior. The results of this study, in which b-catenin transgenic mice exhibited behaviors identical to those observed in lithium-treated mice, are consistent with the hypothesis that the behavioral effects of lithium in these models are mediated through its direct inhibition of GSK-3 and the consequent increase in b-catenin. By associating the behavioral effects of lithium with b-catenin levels, these data suggest that increasing b-catenin might be a novel therapeutic strategy for mood disorders.

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“…Signal-induced accumulation of Arm/␤-catenin results from an interruption of its normal turnover mediated by ubiquitination/proteasomal degradation. This degradation turnover necessitates the phosphorylation of several residues of the Arm N-terminus (Peifer et al, 1994). The kinase Shaggy (Sgg), the Drosophila GSK-3 ortholog, is an antagonist of Wg signal transduction and was shown critical for the phosphorylations and subsequent ubiquination-marking of Arm/␤-catenin and for the integrity of the Arm/␤-catenin degradation-complex (Hart et al, 1999;Liu et al, 2002).…”

mentioning

confidence: 99%

Targeted increase in shaggy activity levels blocks wingless signaling

Bourouis

2002

Genesis

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Phosphorylation of the Drosophila Adherens Junction Protein Armadillo: Roles for Wingless Signal and Zeste-white 3 Kinase

Cited by 230 publications

References 0 publications

Wingless signaling modulates cadherin-mediated cell adhesion inDrosophilaimaginal disc cells

Wingless signaling modulates cadherin-mediated cell adhesion inDrosophilaimaginal disc cells

β-Catenin Overexpression in the Mouse Brain Phenocopies Lithium-Sensitive Behaviors

Targeted increase in shaggy activity levels blocks wingless signaling

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