Spatial regulation of expanded transcription in the Drosophila wing imaginal disc

Lan-Hsin Wang,Nicholas E. Baker,Esther Marianna Verheyen

doi:10.1371/journal.pone.0201317

Lan-Hsin Wang, Nicholas E. Baker + Show 1 more

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https://doi.org/10.1371/journal.pone.0201317

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Abstract

Growth and patterning are coordinated during development to define organ size and shape. The growth, proliferation and differentiation of Drosophila wings are regulated by several conserved signaling pathways. Here, we show that the Salvador-Warts-Hippo (SWH) and Notch pathways converge on an enhancer in the expanded (ex) gene, which also responds to levels of the bHLH transcription factor Daughterless (Da). Separate cis-regulatory elements respond to Salvador-Warts-Hippo (SWH) and Notch pathways, to bHLH proteins, and to unidentified factors that repress ex transcription in the wing pouch and in the proneural region at the anterior wing margin. Senseless, a zinc-finger transcription factor acting in proneural regions, had a negative impact on ex transcription in the proneural region, but the transcriptional repressor Hairy had no effect. Our study suggests that a complex pattern of ex transcription results from integration of a uniform SWH signal with multiple other inputs, rather than from a pattern of SWH signaling.

Highlights

One Drosophila gene that integrates signals from multiple growth pathways is expanded [1,2,3,4]
These results suggest that N represses ex transcription in the wing pouch through region E of the enhancer
Because Da protein is elevated in all proneural regions yet examined, yet at the anterior wing margin this does not seem to elevate ex transcription, we examined some other proneural regions for comparison

Summary

Introduction

One Drosophila gene that integrates signals from multiple growth pathways is expanded [1,2,3,4]. The ex gene encodes a FERM-domain protein that activates the Salvador-Warts-Hippo (SWH) pathway of tumor suppressors by at least two mechanisms. Binding of Ex with another FERM domain-containing protein Schip can recruit the Hippo (Hpo) kinase Tao-1 and phosphorylates Hpo [7]. Phosphorylation of Hpo, and Warts, leads to the phosphorylation and cytoplasmic retention of Yki. Phosphorylation of Hpo, and Warts, leads to the phosphorylation and cytoplasmic retention of Yki Both mechanisms of cytoplasmic Yki retention prevent the expression of growth and survival genes including cyclin E, diap, and bantam by this transcriptional coactivator [8,9,10,11,12,13,14,15]

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