l(3)10512
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
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
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
4.565 (compiled cDNA)
4.489 (compiled cDNA)
None of the polypeptides share 100% sequence identity.
924 (aa)
949 (aa); 150 (kD observed)
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.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: reported as salivary gland anlage
Comment: reported as tracheal system anlage
Comment: reported as salivary gland primordium
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.
trh transcripts are expressed initially in the trahceal placodes, tracheal pits, and in salivary placodes. Later, they are expressed in migrating tracheal cells.
Protein is detected in 10 ectodermal placodes along each dorsal-lateral side of the embryo.
trh protein is detected in the nuclei of all tracheal cells. Staining is also observed in the salivary gland ducts and cells that will give rise to the posterior spiracles. Weak staining is seen in salivary glands.
JBrowse - Visual display of RNA-Seq signals
View Dmel\trh in JBrowsePlease 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 JBrowse 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.
polyclonal
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.
trh induces tracheal cell fates.
The PAS domain of trh confers its target gene specificity.
The trh product is required for tubulogenesis.
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.
The autosomal "FLP-DFS" technique (using the P{ovoD1-18} P{FRT(whs)} P{hsFLP} chromosomes) has been used to study the zygotic lethal mutation.
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.
trh mutants display no tracheae and the filzkorper are not elongated.
Source for merge of: CG13885 HDC07747
Source for merge of: trh CG13885
Annotations CG6883 and CG13885 merged as CG42865 in release 5.30 of the genome annotation.