Wingless signaling modulates cadherin-mediated cell adhesion in<i>Drosophila</i>imaginal disc cells

Wodarz, Andreas; Stewart, Daniel B.; Nelson, W. James; Nusse, Roel

doi:10.1242/jcs.02973

Cited by 31 publications

(31 citation statements)

References 56 publications

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“…They further reported that DE-cad overexpression clones apically constricted, suggesting a causal relationship between Wnt pathway activation, elevated DE-cad, and apical constriction (Jaiswal et al, 2006). Others have also reported that DE-cad is a transcriptional target of Wnt signaling (Wodarz et al, 2006). Together, this suggested that at least some of the APC null morphological changes could be due to Wnt-mediated upregulation of DE-cad .…”

Section: Resultsmentioning

confidence: 99%

Apical constriction and invagination downstream of the canonical Wnt signaling pathway require Rho1 and Myosin II

Zimmerman

Thorpe

Medrano

et al. 2010

Developmental Biology

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The tumor suppressor Adenomatous polyposis coli (APC) is a negative regulator of Wnt signaling and functions in cytoskeletal organization. Disruption of human APC in colonic epithelia initiates benign polyps that progress to carcinoma following additional mutations. The early events of polyposis are poorly understood, as is the role of canonical Wnt signaling in normal epithelial architecture and morphogenesis. To determine the consequences of complete loss of APC in a model epithelium, we generated APC2 APC1 double null clones in the Drosophila wing imaginal disc. APC loss leads to segregation, apical constriction, and invagination that result from transcriptional activation of canonical Wnt signaling. Further, we show that Wnt-dependent changes in cell fate can be decoupled from Wnt-dependent changes in cell shape. Wnt activation is reported to upregulate DE-cadherin in wing discs, and elevated DE-cadherin is thought to promote apical constriction. We find that apical constriction and invagination of APC null tissue are independent of DE-cadherin elevation, but are dependent on Myosin II activity. Further, we show that disruption of Rho1 suppresses apical constriction and invagination in APC null cells. Our data suggest a novel link between canonical Wnt signaling and epithelial structure that requires activation of the Rho1 pathway and Myosin II.

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Section: Resultsmentioning

confidence: 99%

Apical constriction and invagination downstream of the canonical Wnt signaling pathway require Rho1 and Myosin II

Zimmerman

Thorpe

Medrano

et al. 2010

Developmental Biology

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“…For example, in addition to reports of Wnt pathway activation having effects on cadherin function (Bradley et al 1993;Hinck et al 1994b;Hinck et al 1994a;Yanagawa et al 1997;Shariatmadari et al 2005;Ulrich et al 2005;Wodarz et al 2006), there are indications of physical associations between Wnt and cadherin/protocadherin pathway components Qin et al 2005;Hay et al 2009), suggesting that cadherins are likely to modulate canonical (b-catenin mediated) or noncanonical (alternative) Wnt pathways.…”

Section: P120 Subfamilymentioning

confidence: 99%

Junctional Music that the Nucleus Hears: Cell-Cell Contact Signaling and the Modulation of Gene Activity

McCrea

Gu²,

Balda³

2009

Cold Spring Harbor Perspectives in Biology

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“…Furthermore, release of Arm from the AJs, and its stabilization, may also contribute to the activation of Arm. The stimulation of E-cadherin transcription by Src42A may be a direct consequence of Arm activation, as stimulation of E-cadherin synthesis by Wg was observed in cultured Drosophila cells (Wodarz et al, 2006). TCF-dependent synthesis of E-cadherin by itself was not rate limiting for tracheal cell adhesion, probably because its absence left the level of E-cadherin above the threshold to maintain cell adhesion.…”

mentioning

confidence: 97%

Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis

Shindo

Wada²,

Kaido³

et al. 2008

Development

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The downregulation of E-cadherin by Src promotes epithelial to mesenchymal transition and tumorigenesis. However, a simple loss of cell adhesion is not sufficient to explain the diverse developmental roles of Src and metastatic behavior of viral Src-transformed cells. Here, we studied the functions of endogenous and activated forms of Drosophila Src in the context of tracheal epithelial development, during which extensive remodeling of adherens junctions takes place. We show that Src42A is selectively activated in the adherens junctions of epithelia undergoing morphogenesis. Src42A and Src64B are required for tracheal development and to increase the rate of adherens junction turnover. The activation of Src42A caused opposing effects: it reduced the E-cadherin protein level but stimulated transcription of the E-cadherin gene through the activation of Armadillo and TCF. This TCF-dependent pathway was essential for the maintenance of E-cadherin expression and for tissue integrity under conditions of high Src activity. Our data suggest that the two opposing outcomes of Src activation on E-cadherin facilitate the efficient exchange of adherens junctions, demonstrating the key role of Src in the maintenance of epithelial integrity. KEY WORDS:Src, E-cadherin, Armadillo, Drosophila, Trachea, Cancer Development 135, 1355Development 135, -1364Development 135, (2008Development 135, ) doi:10.1242 Riken Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku Kobe 650-0047, Japan. DEVELOPMENT 1356 strain carrying the trachea-specific btl-Gal4 driver and the UAS-GFPmoesin marker. An additional 142 lines lacking the rough eye phenotype were also tested. GS11022 (Src42A) and GS9618 (Src64B) were analyzed for further study. Fly stocks and geneticsWe used strong loss-of-function alleles of Src genes: Src42A 26-1 (Takahashi et al., 2005), Src42A myri (Tateno et al., 2000) and Src64B P1 (Dodson et al., 1998). The following strains were used in this study: trachealess enhancer trap line 1-eve-1 (Perrimon et al., 1991), UAS-wg (Lawrence et al., 1995), UAS-arm S10 (Pai et al., 1997), UAS-TCF⌬N (van de Wetering et al., 1997), UAS-E-cadherin-GFP (Oda and Tsukita, 1999b), UAS-D␣-catenin-GFP (Oda and Tsukita, 1999a), shg-lacZ , UAS-GFP-moesin (Chihara et al., 2003), YF (Tateno et al., 2000), UAS-Src42A-RNAi (NIG Stock Center) and btl-Gal4 (Shiga et al., 1996). Src42A DN was constructed by introducing the K295M mutation at the catalytic center of the kinase domain and was cloned into the pUAST vector (Brand and Perrimon, 1993). Immunostaining and imagingThe following primary antibodies were used: rat anti-Esg (Fuse et al., 1994); mouse anti-tracheal luminal antigen 2A12, mouse anti-Armadillo N27A1 and mouse anti-septin 4C9H4 (Developmental Studies Hybridoma Bank); rabbit anti-␤-galactosidase (Cappel); mouse anti-GFP B-2 and rabbit anti-GFP (MBL); rabbit anti-Src PY418 (Biosource International); rat anti-E-cadherin (DCAD2) (Oda et al., 1994) and rabbit anti-Src42A (Takahashi et al., 2005). Chicken anti-Src42A antibody ...

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Wingless signaling modulates cadherin-mediated cell adhesion inDrosophilaimaginal disc cells

Cited by 31 publications

References 56 publications

Apical constriction and invagination downstream of the canonical Wnt signaling pathway require Rho1 and Myosin II

Apical constriction and invagination downstream of the canonical Wnt signaling pathway require Rho1 and Myosin II

Junctional Music that the Nucleus Hears: Cell-Cell Contact Signaling and the Modulation of Gene Activity

Dual function of Src in the maintenance of adherens junctions during tracheal epithelial morphogenesis

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