Welcome to the new version of CaltechAUTHORS. Login is currently restricted to library staff. If you notice any issues, please email coda@library.caltech.edu
Published February 1, 2015 | Published + Supplemental Material
Journal Article Open

Ectopic Expression Screen Identifies Genes Affecting Drosophila Mesoderm Development Including the HSPG Trol

Abstract

Gastrulation of the embryo involves coordinate cell movements likely supported by multiple signaling pathways, adhesion molecules, and extracellular matrix components. Fibroblast growth factors (FGFs) have a major role in Drosophila melanogaster mesoderm migration, however few other inputs are known and the mechanism supporting cell movement is unclear. To provide insight, we carried out an ectopic expression screen to identify secreted or membrane-associated molecules that act to support mesoderm migration. Twenty-four UAS insertions were identified that cause lethality when expressed in either the mesoderm (Twi-Gal4) or ectoderm (69B-Gal4). The list was narrowed to a subset of ten genes that were shown to exhibit loss-of-function mutant phenotypes specifically affecting mesoderm migration. These include the FGF ligand Pyramus, α-integrins, E-cadherin, Cueball, EGFR, JAK/STAT signaling components, as well as the heparan sulfate proteoglycan (HSPG) Terribly reduced optic lobes (Trol). Trol encodes the ortholog of mammalian HSPG Perlecan, a demonstrated FGF signaling cofactor. Here we examine the role of Trol in Drosophila mesoderm migration and compare and contrast its role with that of Syndecan (Sdc), another HSPG, previously implicated in this process. Embryos mutant for Trol or Sdc were obtained and analyzed. Our data support the view that both HSPGs function to support FGF-dependent processes in the early embryo as they share phenotypes with FGF mutants: Trol in terms of effects on mesoderm migration and caudal visceral mesoderm (CVM) migration, and Sdc in terms of dorsal mesoderm specification. The differential roles uncovered for these two HSPGs suggest that HSPG cofactor choice may modify FGF-signaling outputs.

Additional Information

© 2014 Author et al. This is an open-access article distributed under the terms of the Creative Commons Attribution Unported License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Received November 24, 2014. Accepted December 22, 2014. We are grateful to the Zinn lab (Caltech) for sharing their CSS insertion fly stock collection and Marc Freeman, Stephen Crews, and Manfred Frasch for sharing additional fly stocks and antibodies. We also would like to thank Kai Zinn for helpful discussions, Young-Kyung Bae for sharing unpublished results, and Man Ho Wong and Molly Lichten for their invaluable help with the screen. This work was funded by a grant to A.S. from the NIH/NIGMS R01GM104838.

Attached Files

Published - 301.full.pdf

Supplemental Material - 015891SI.pdf

Supplemental Material - FigureS2.pdf

Supplemental Material - FigureS3.pdf

Supplemental Material - TableS1.pdf

Files

FigureS2.pdf
Files (5.7 MB)
Name Size Download all
md5:d2c44566336b03480d22bf9aef422668
279.0 kB Preview Download
md5:57e84d010fb44392c373cfa517495352
145.2 kB Preview Download
md5:51294e7ddf4a03e167dc24cfb289d90e
226.3 kB Preview Download
md5:9c14aba77e491582f773193bec6bd8a3
765.5 kB Preview Download
md5:eb350bc50934c893eae712829f5aa556
4.2 MB Preview Download

Additional details

Created:
August 22, 2023
Modified:
October 19, 2023