Abstract

BackgroundThe coordinated action of genes that control patterning, cell fate determination, cell size, and cell adhesion is required for proper wing formation in Drosophila. Defects in any of these basic processes can lead to wing aberrations, including blisters. The xenicid mutation was originally identified in a screen designed to uncover regulators of adhesion between wing surfaces [1].Principal FindingsHere, we demonstrate that expression of the βPS integrin or the patterning protein Engrailed are not affected in developing wing imaginal discs in xenicid mutants. Instead, expression of the homeotic protein Ultrabithorax (Ubx) is strongly increased in xenicid mutant cells.ConclusionOur results suggest that upregulation of Ubx transforms cells from a wing blade fate to a haltere fate, and that the presence of haltere cells within the wing blade is the primary defect leading to the adult wing phenotypes observed.

Highlights

  • Wing development in Drosophila depends on intricate coordination of complex developmental processes, including cell fate determination, growth, and adhesion

  • Our results suggest that upregulation of Ubx transforms cells from a wing blade fate to a haltere fate, and that the presence of haltere cells within the wing blade is the primary defect leading to the adult wing phenotypes observed

  • None of the other integrin subunits or ECM ligands is located near Additional Sex Combs (Asx) chromosomal binding sites in salivary gland polytene chromosomes [18]. These results suggest that Asx mutant defects in the wing are not due to changes in integrin expression or function in the developing wing disc

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Summary

Introduction

Wing development in Drosophila depends on intricate coordination of complex developmental processes, including cell fate determination, growth, and adhesion. The blade of the wing is formed when the disc folds on itself and telescopes out, after axes are established and the majority of cell divisions have occurred. Signals that control axis formation, patterning, cell division, and adhesion during wing formation have been identified. In the Drosophila wing imaginal disc, three axes are defined by earlyexpressed signals. These axes provide wing cells with positional information used for cell fate determination. The coordinated action of genes that control patterning, cell fate determination, cell size, and cell adhesion is required for proper wing formation in Drosophila. The xenicid mutation was originally identified in a screen designed to uncover regulators of adhesion between wing surfaces [1]

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