SoxNeuro and Shavenbaby act cooperatively to shape denticles in the embryonic epidermis of Drosophila.

Loading...
Thumbnail Image

Date

2017-06-15

Journal Title

Journal ISSN

Volume Title

Repository Usage Stats

199
views
140
downloads

Citation Stats

Abstract

During development, extracellular signals are integrated by cells to induce the transcriptional circuitry that controls morphogenesis. In the fly epidermis, Wingless (Wg)/Wnt signaling directs cells to produce either a distinctly shaped denticle or no denticle, resulting in a segmental pattern of denticle belts separated by smooth, or 'naked', cuticle. Naked cuticle results from Wg repression of shavenbaby (svb), which encodes a transcription factor required for denticle construction. We have discovered that although the svb promoter responds differentially to altered Wg levels, Svb alone cannot produce the morphological diversity of denticles found in wild-type belts. Instead, a second Wg-responsive transcription factor, SoxNeuro (SoxN), cooperates with Svb to shape the denticles. Co-expressing ectopic SoxN with svb rescued diverse denticle morphologies. Conversely, removing SoxN activity eliminated the residual denticles found in svb mutant embryos. Furthermore, several known Svb target genes are also activated by SoxN, and we have discovered two novel target genes of SoxN that are expressed in denticle-producing cells and that are regulated independently of Svb. We conclude that proper denticle morphogenesis requires transcriptional regulation by both SoxN and Svb.

Department

Description

Provenance

Citation

Published Version (Please cite this version)

10.1242/dev.150169

Publication Info

Rizzo, Nicholas P, and Amy Bejsovec (2017). SoxNeuro and Shavenbaby act cooperatively to shape denticles in the embryonic epidermis of Drosophila. Development, 144(12). pp. 2248–2258. 10.1242/dev.150169 Retrieved from https://hdl.handle.net/10161/15039.

This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.

Scholars@Duke

Bejsovec

Amy Bejsovec

Associate Professor of Biology

My laboratory explores the molecular mechanisms of pattern formation in developing embryos. We focus on the Wingless(Wg)/Wnt class of secreted growth factor: these molecules promote cell-cell communication leading to important cell fate decisions during the development of both vertebrate and invertebrate embryos. In addition, this highly conserved pathway is essential for maintaining stem cell populations and is associated with human cancers when inappropriately activated in adult tissues. Wg/Wnt molecules have proven difficult to work with biochemically because they associate tightly with cell membranes. Therefore, we exploit the powerful genetic and molecular techniques available in Drosophila to approach basic questions about Wg/Wnt signal transduction.

Current work in the lab includes analysis of genes discovered as suppressors or enhancers of wg mutant phenotypes, which may identify new control mechanisms for the pathway. In earlier work, we found that the Wg-activated transcription factor, dTCF, can act as either a repressor or an activator of Wg target genes, and our screens have uncovered other factors that may influence this genetic switch. We have also characterized a Drosophila homolog of the human tumor suppressor, APC, which negatively regulates the Wg/Wnt signaling pathway, and we are currently studying other genes that show similar properties. We use cultured human cells to determine whether gene activities we have discovered and characterized in the fly embryo are relevant to the mammalian Wnt pathway as well.


Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.