Author Correction: Asymmetric requirement of Dpp/BMP morphogen dispersal in the Drosophila wing disc

Gap junctions are intercellular junctions found in both vertebrates and invertebrates through which ions and small molecules can pass. Their distribution in tissues could be of critical importance for ionic coupling or metabolic cooperation between cells or for regulating the intracellular movement of growth control and pattern formation factors. Studies of the distribution of gap junctions in mutants which develop abnormally may shed light upon their role in normal development. I report here the distribution of gap junctions in the wing pouch of 3 Drosophila wing disc mutants, vg (vestigial) a cell death mutant, 1(2)gd (lethal giant disc) a pattern abnormality mutant and 1(2)gl (lethal giant larva) a neoplastic mutant and compare these with wildtype wing discs.The wing pouch (the anlagen of the adult wing blade) of a wild-type wing disc is shown in Fig. 1 and consists of columnar cells (Fig. 5) joined by gap junctions (Fig. 6). 14000x EMs of conventionally processed, UA en bloc stained, longitudinally sectioned wing pouches were enlarged to 45000x with a projector and tracings were made on which the lateral plasma membrane (LPM) and gap junctions were marked.

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Faculty Opinions recommendation of Extrusion of cells with inappropriate Dpp signaling from Drosophila wing disc epithelia.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1024714.293712 ◽

2005 ◽

Author(s):

Marta Llimargas

Keyword(s):

Wing Disc ◽

Drosophila Wing

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Faculty Opinions recommendation of Pins is not required for spindle orientation in the Drosophila wing disc.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726415490.793533433 ◽

2017 ◽

Author(s):

Ian Macara

Keyword(s):

Wing Disc ◽

Spindle Orientation ◽

Drosophila Wing

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Faculty Opinions recommendation of Cycd/cdk4 and discontinuities in dpp signaling activate TORC1 in the drosophila wing disc.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.729075168.793536162 ◽

2017 ◽

Author(s):

Julien Sage

Keyword(s):

Wing Disc ◽

Drosophila Wing

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Regeneration from duplicating fragments of the Drosophila wing disc

Development ◽

10.1242/dev.66.1.117 ◽

1981 ◽

Vol 66 (1) ◽

pp. 117-126

Author(s):

Jane Karlsson ◽

R. J. Smith

Keyword(s):

Imaginal Disc ◽

General Rule ◽

Wing Disc ◽

The Other ◽

Posterior Compartment ◽

Drosophila Wing ◽

Polar Coordinate ◽

New Type ◽

Coordinate Model

It is a general rule that of two complementary Drosophila imaginal disc fragments, one regenerates and the other duplicates. This paper reports an investigation of an exception to this rule. Duplicating fragments from the periphery of the wing disc which lacked presumptive notum were found to regenerate notum structures during and after duplication. The propensity for this was greatest in fragments lying close to the presumptive notum, with the exception of a fragment confined to the posterior compartment, which did not regenerate notum. Structures were added sequentially, and regeneration stopped once most of the notum was present. These results are not easily explained by the polar coordinate model, which states that regeneration cannot occur from duplicating fragments. Since compartments appear to be involved in this type of regeneration as in others, it is suggested that a new type of model is required, one which permits simultaneous regeneration and duplication, and assigns a major role to compartments.

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Endocytosis of Wingless via a dynamin-independent pathway is necessary for signaling in Drosophila wing discs

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1610565113 ◽

2016 ◽

Vol 113 (45) ◽

pp. E6993-E7002 ◽

Cited By ~ 10

Author(s):

Anupama Hemalatha ◽

Chaitra Prabhakara ◽

Satyajit Mayor

Keyword(s):

Signal Transduction ◽

Wing Disc ◽

Low Ph ◽

Endocytic Pathway ◽

Apical Surface ◽

Receptor Complexes ◽

Drosophila Wing ◽

Wing Discs ◽

Ph Dependent ◽

Endocytic Pathways

Endocytosis of ligand-receptor complexes regulates signal transduction during development. In particular, clathrin and dynamin-dependent endocytosis has been well studied in the context of patterning of the Drosophila wing disc, wherein apically secreted Wingless (Wg) encounters its receptor, DFrizzled2 (DFz2), resulting in a distinctive dorso-ventral pattern of signaling outputs. Here, we directly track the endocytosis of Wg and DFz2 in the wing disc and demonstrate that Wg is endocytosed from the apical surface devoid of DFz2 via a dynamin-independent CLIC/GEEC pathway, regulated by Arf1, Garz, and class I PI3K. Subsequently, Wg containing CLIC/GEEC endosomes fuse with DFz2-containing vesicles derived from the clathrin and dynamin-dependent endocytic pathway, which results in a low pH-dependent transfer of Wg to DFz2 within the merged and acidified endosome to initiate Wg signaling. The employment of two distinct endocytic pathways exemplifies a mechanism wherein cells in tissues leverage multiple endocytic pathways to spatially regulate signaling.

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Role of the EGF receptor pathway in growth and patterning of the Drosophila wing through the regulation of vestigial

Development ◽

10.1242/dev.126.5.975 ◽

1999 ◽

Vol 126 (5) ◽

pp. 975-985 ◽

Cited By ~ 6

Author(s):

R. Nagaraj ◽

A.T. Pickup ◽

R. Howes ◽

K. Moses ◽

M. Freeman ◽

...

Keyword(s):

Egf Receptor ◽

Regulatory Gene ◽

Ectopic Expression ◽

Wing Disc ◽

Loss Of Function ◽

Drosophila Wing ◽

Expression Studies ◽

Coordinated Expression ◽

Wing Pouch

Growth and patterning of the Drosophila wing disc depends on the coordinated expression of the key regulatory gene vestigial both in the Dorsal-Ventral (D/V) boundary cells and in the wing pouch. We propose that a short-range signal originating from the core of the D/V boundary cells is responsible for activating EGFR in a zone of organizing cells on the edges of the D/V boundary. Using loss-of-function mutations and ectopic expression studies, we show that EGFR signaling is essential for vestigial transcription in these cells and for making them competent to undergo subsequent vestigial-mediated proliferation within the wing pouch.

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Control of growth and patterning of the Drosophila wing imaginal disc by EGFR-mediated signaling

Development ◽

10.1242/dev.129.6.1369 ◽

2002 ◽

Vol 129 (6) ◽

pp. 1369-1376 ◽

Cited By ~ 2

Author(s):

Myriam Zecca ◽

Gary Struhl

Keyword(s):

Gene Expression ◽

Imaginal Disc ◽

Ectopic Expression ◽

Growth Factor Receptor ◽

Wing Disc ◽

Wing Imaginal Disc ◽

Egfr Signaling ◽

Drosophila Wing ◽

Compartment Boundary ◽

Egfr Ligand

The subdivision of the Drosophila wing imaginal disc into dorsoventral (DV) compartments and limb-body wall (wing-notum) primordia depends on Epidermal Growth Factor Receptor (EGFR) signaling, which heritably activates apterous (ap) in D compartment cells and maintains Iroquois Complex (Iro-C) gene expression in prospective notum cells. We examine the source, identity and mode of action of the EGFR ligand(s) that specify these subdivisions. Of the three known ligands for the Drosophila EGFR, only Vein (Vn), but not Spitz or Gurken, is required for wing disc development. We show that Vn activity is required specifically in the dorsoproximal region of the wing disc for ap and Iro-C gene expression. However, ectopic expression of Vn in other locations does not reorganize ap or Iro-C gene expression. Hence, Vn appears to play a permissive rather than an instructive role in organizing the DV and wing-notum segregations, implying the existance of other localized factors that control where Vn-EGFR signaling is effective. After ap is heritably activated, the level of EGFR activity declines in D compartment cells as they proliferate and move ventrally, away from the source of the instructive ligand. We present evidence that this reduction is necessary for D and V compartment cells to interact along the compartment boundary to induce signals, like Wingless (Wg), which organize the subsequent growth and differentiation of the wing primordium.

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