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| Status |
Public on Dec 21, 2011 |
| Title |
Trachealess (Trh) regulates all tracheal genes during Drosophila embryogenesis |
| Organism |
Drosophila melanogaster |
| Experiment type |
Expression profiling by array
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| Summary |
Abstract: The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, suggesting that there are additional targets. To identify uncharacterized transcriptional targets of Trh and to further understand the role of Trh in embryonic tracheal formation, we performed an in situ hybridization screen using a library of ~100 tracheal-expressed genes identified by the Berkeley Drosophila Genome Project (BDGP). Surprisingly, expression of every tracheal gene we tested was dependent on Trh, suggesting a major role for Trh in activation and maintenance of tracheal gene expression. A re-examination of the interdependence of the known early-expressed transcription factors, including trh, ventral veinless (vvl) and knirps/knirps-related (kni/knrl), suggests a new model for how gene expression is controlled in the trachea, with trh regulating expression of vvl and kni, but not vice versa. A pilot screen for the targets of Vvl and Kni/Knrl revealed that Vvl and Kni have only minor roles compared to Trh. Finally, genome-wide microarray experiments identified additional Trh targets and revealed that a of biological processes are affected by the loss of trh.
Goals: The goals of the microarray experiments were to identify additional targets of the Trh transcription factor to learn the range of genes regulated by this transcription factor during embryogenesis. Our in situ screen revealed that Trh is required for all tested tracheal genes. Our new data now shows that Trh affects a range of biological processes.
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| Overall design |
RNA was isolated from stage 11-16 wild type Drosophila embryos and compared to RNA from trh null mutant embryos of the same age; all samples were hybridized to the Drosophila Genome 2.0 Affymetrix array. Three individual replicates were obtained for each sample.
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| Contributor(s) |
Chung S, Andrew DJ |
| Citation(s) |
21963537 |
| Submission date |
Apr 21, 2011 |
| Last update date |
Aug 28, 2018 |
| Contact name |
Deborah J Andrew |
| E-mail(s) |
dandrew@jhmi.edu
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| Organization name |
Johns Hopkins University School of Medicine
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| Department |
Cell Biology
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| Street address |
725 N. Wolfe St., Hunterian G-1
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| City |
Baltimore |
| State/province |
MD |
| ZIP/Postal code |
21205 |
| Country |
USA |
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| Platforms (1) |
| GPL1322 |
[Drosophila_2] Affymetrix Drosophila Genome 2.0 Array |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA138679 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE28780_RAW.tar |
12.1 Mb |
(http)(custom) |
TAR (of CEL) |
| Processed data included within Sample table |
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