Regulation of Wingless and Vestigial expression in wing and haltere discs of<i>Drosophila</i>

Mohit, Prasad; Bajpai, Ruchi; Shashidhara, L. S.

doi:10.1242/dev.00393

Cited by 34 publications

(22 citation statements)

References 48 publications

(64 reference statements)

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“…1C) based on immunolocalization of DE-Cad and ␤-catenin/Arm besides binding with fluorochrome conjugated Phalloidin to F-actin. Both ␤-catenin/Arm (Collins and Treisman, 2000;Jiang and Struhl, 1998;Prasad et al, 2003) and DE-Cad display characteristic upregulation across the DV boundary along the PD axis of wing imaginal disc ( Fig. 1D-DЈЈ).…”

Section: Resultsmentioning

confidence: 97%

“…Following stocks were used: ft fd (ft 8 ) (Mahoney et al, 1991), ft 422 (Rawls et al, 2002), UAS-arm S10 , UAS-arm S2 (Pai et al, 1997), UAS-dsh (Neumann and Cohen, 1996), UAS-DE-Cad (Greaves et al, 1999), UAS-tcf⌬N (van de Wetering et al, 1997), UAS-ft (Matakatsu and Blair, 2004), UAS-GPI::DFz2 (Cadigan et al, 1998), N23-Gal4 (Prasad et al, 2003), vg-Gal4 (Simmonds et al, 1995). Q-vg-lacZ (Kim et al, 1996), BE-vg-lacZ (Williams et al, 1994) and fz…”

Section: Fly Stocks and Geneticsmentioning

confidence: 99%

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Fat and Wingless signaling oppositely regulate epithelial cell-cell adhesion and distal wing development inDrosophila

2006

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Development of organ-specific size and shape demands tight coordination between tissue growth and cell-cell adhesion. Dynamic regulation of cell adhesion proteins thus plays an important role during organogenesis. In Drosophila, the homophilic cell adhesion protein DE-Cadherin (DE-Cad)regulates epithelial cell-cell adhesion at adherens junctions (AJs). Here, we show that along the proximodistal (PD) axis of the developing wing epithelium,apical cell shapes and expression of DE-Cad are graded in response to Wingless (Wg), a morphogen secreted from the dorsoventral (DV) organizer in distal wing, suggesting a PD gradient of cell-cell adhesion. The Fat (Ft)tumor suppressor, by contrast, represses DE-Cad expression. In genetic tests, ft behaves as a suppressor of Wg signaling. Cytoplasmic pool of β-catenin/Arm, the intracellular transducer of Wg signaling, is negatively correlated with the activity of Ft. Moreover, unlike that of Wg, signaling by Ft negatively regulates the expression of Distalless(Dll) and Vestigial (Vg). Finally, we show that Ft intersects Wnt/Wg signaling, downstream of the Wg ligand. Fat and Wg signaling thus exert opposing regulation to coordinate cell-cell adhesion and patterning along the PD axis of Drosophila wing.

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Section: Resultsmentioning

confidence: 97%

Section: Fly Stocks and Geneticsmentioning

confidence: 99%

Fat and Wingless signaling oppositely regulate epithelial cell-cell adhesion and distal wing development inDrosophila

2006

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“…Our analysis has identified all genes previously showed as direct Ubx targets in the haltere pouch as well as a large fraction of suspected Ubx targets: spalt, knot, blistered, and vestigial (17,(19)(20)(21); anachronism, CG16884, CG7201, CG8780, and CG11641 (27); the Egf receptor pathway components vein, rhomboid, and kekkon-1 (22); Cyp310a1, Delta, CG10990, CG5171, and E(spl)-C genes (26); and dally and dally-like (14,(23)(24)(25). Most of the targets identified in our microarray analysis have not been studied thoroughly in the context of wing or haltere development, but some of these genes have been reported in microarray studies and genetic screens (31,32).…”

Section: Discussionmentioning

confidence: 99%

“…Molecular genetic studies have shown that many key patterning genes in the larval wing primordium are indeed regulated by Ubx, directly or indirectly, in the haltere primordium (14,17,(19)(20)(21)(22)(23)(24)(25). This finding has prompted the use of microarray expression profiling to systematically identify differentially expressed genes between wing and haltere imaginal discs (26,27).…”

mentioning

confidence: 99%

Hox gene Ultrabithorax regulates distinct sets of target genes at successive stages of Drosophila haltere morphogenesis

Pavlopoulos

Akam

2011

Proc. Natl. Acad. Sci. U.S.A.

109

125

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Hox genes encode highly conserved transcription factors that regionalize the animal body axis by controlling complex developmental processes. Although they are known to operate in multiple cell types and at different stages, we are still missing the batteries of genes targeted by any one Hox gene over the course of a single developmental process to achieve a particular cell and organ morphology. The transformation of wings into halteres by the Hox gene Ultrabithorax (Ubx) in Drosophila melanogaster presents an excellent model system to study the Hox control of transcriptional networks during successive stages of appendage morphogenesis and cell differentiation. We have used an inducible misexpression system to switch on Ubx in the wing epithelium at successive stages during metamorphosis-in the larva, prepupa, and pupa. We have then used extensive microarray expression profiling and quantitative RT-PCR to identify the primary transcriptional responses to Ubx. We find that Ubx targets range from regulatory genes like transcription factors and signaling components to terminal differentiation genes affecting a broad repertoire of cell behaviors and metabolic reactions. Ubx up-and downregulates hundreds of downstream genes at each stage, mostly in a subtle manner. Strikingly, our analysis reveals that Ubx target genes are largely distinct at different stages of appendage morphogenesis, suggesting extensive interactions between Hox genes and hormone-controlled regulatory networks to orchestrate complex genetic programs during metamorphosis.appendage specialization | homeotic genes | serial homology

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“…When both Sgg/ GSK-3b and hAPC are misexpressed together, human APC fails to sequester ARM/b-catenin (Bhandari and Shashidhara, 2001). This behavior has been validated in different genetic backgrounds of increased or decreased levels of Sgg/GSK-3b activity (Prasad et al, 2003;Bajpai et al, 2004). The previous observations suggest that at low levels of Sgg/GSK-3b activity, overexpressed hAPC binds and sequesters ARM/b-catenin, while at high levels of Sgg/GSK-3b activity, overexpressed hAPC binds and degrades ARM/b-catenin.…”

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confidence: 89%

Human APC sequesters β-catenin even in the absence of GSK-3β in a Drosophila model

2007

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There have been conflicting reports on the requirement of GSK-3b-mediated phosphorylation of the tumor suppressor adenomatous polyposis coli (APC) vis-a`-vis its ability to bind and degrade b-catenin. Using a unique combination of loss of function for Shaggy/GSK-3b and a gain of function for human APC in Drosophila, we show that misexpressed human APC (hAPC) can still sequester Armadillo/b-catenin. In addition, human APC could suppress gain of Wnt/Wingless phenotypes associated with loss of Shaggy/GSK-3b activity, suggesting that sequestered Armadillo/b-catenin is non-functional. Based on these studies, we propose that binding per se of b-catenin by APC does not require phosphorylation by GSK-3b.

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Regulation of Wingless and Vestigial expression in wing and haltere discs ofDrosophila

Cited by 34 publications

References 48 publications

Fat and Wingless signaling oppositely regulate epithelial cell-cell adhesion and distal wing development inDrosophila

Fat and Wingless signaling oppositely regulate epithelial cell-cell adhesion and distal wing development inDrosophila

Hox gene Ultrabithorax regulates distinct sets of target genes at successive stages of Drosophila haltere morphogenesis

Human APC sequesters β-catenin even in the absence of GSK-3β in a Drosophila model

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