bHLH-PAS nuclear transcription factor required for the formation of the tube of the salivary duct, trachea and filzkorper - required for expression of all tracheal genes - mutants exhibit a defect in the ability of the tracheal precursors to organize tubes, the same defect seen in salivary glands
Gene model reviewed during 5.44
Stop-codon suppression (UAG) postulated; FBrf0216884.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.46
Gene model reviewed during 5.56
None of the polypeptides share 100% sequence identity.
Efficient DNA binding requires dimerization with another bHLH protein. Heterodimer with tgo.
Ser-673 phosphorylation by PKB/Akt1 is required for nuclear targeting and transcriptional activity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\trh using the Feature Mapper tool.
In situ hybridization with probes specific to the three isoforms of trh show that all display similar expression patterns in the embryo. Expression is observed in the tube-forming cells of the salivary duct, trachea, and filzkorper, and in a subset of cells in the central nervous system.
trh transcripts are detected in the entire salivary gland primordia by embryonic stage 9 but disappear from the secretory cells during stage 12. Expression in tracheal cells begins in stage 8 and continues throughout embryogenesis. trh is expressed in the cells that connect the trachea to the posterior spiracles (which will form the filzkorper) starting in stage 11. It is also expressed in a subset of CNS cells.
Protein is detected in 10 ectodermal placodes along each dorsal-lateral side of the embryo.
GBrowse - Visual display of RNA-Seq signalsView Dmel\trh in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Annotations CG6883 and CG13885 merged as CG42865 in release 5.30 of the genome annotation.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of trh results in reduction of the dendritic field size of ddaE and ddaD neurons. There is a minor reduction in both primary branch outgrowth and the number of lateral branches and a more marked reduction in the overall length of lateral branches. Consequently, the most distal regions of the dendritic field are not innervated. RNAi also causes defects in muscle, defects in dendrite morphogenesis but does not cause obvious defects in da dendrite development.
Annotation CG13885 restored in release 4.3 of the genome annotation.
Annotation CG13885 was eliminated in release 3 of the genome annotation, October 2002.
sim and trh activate transcription by forming dimers with the tgo protein. Gene dosage studies reveal in vivo interactions between sim and tgo, and trh and tgo. The interacting proteins in vivo control CNS midline and tracheal transcription and development.
The distinction between pregland and preduct cells is made by the combination of two spatially separated negative regulatory steps: the Egfr signaling pathway represses fkh in the preduct cells and fkh represses duct specific genes in the pregland cells. trh is a duct-specific gene activator and is one of the targets of fkh repression.
trh encodes a bHLH-PAS protein that is an inducer of tracheal cell fates. Expression is first induced by exogenous cues and is subsequently autoregulated. The role of trh in the formation of several tubular tissues in the embryo suggests it may induce a general fate of branched tubular structures of epithelial origin.