Disease relevance of trh

• Minimal inhibitory concentration values against mainly Gram-negative bacteria ranged from 3.1 to 100 mum [1].

High impact information on trh

• A single 3.1 kb Pax 1 (paired box gene) transcript was detected during embryonic development, whereas no transcripts were detected in adult tissues [2].
• The 3.1 angstrom crystal structure reveals a bound phosphate and patches of positive charge, which may represent the lipopolysaccharide binding site, and a new and unexpected arrangement of four immunoglobulin-like domains forming a horseshoe [3].
• The RhoGAP crossveinless-c links trachealess and EGFR signaling to cell shape remodeling in Drosophila tracheal invagination [4].
• Trachealess (Trh) and Single-minded (Sim) are highly similar Drosophila bHLH/PAS transcription factors [5].
• In trh mutants, tube-forming cells of the salivary gland, trachea, and filzkörper fail to invaginate to form tubes and remain on the embryo surface [6].

Biological context of trh

• The downregulation of Trachealess is dependent on dysfusion function [7].
• Co-expression assays of trachealess and tgo in the developing eye imaginal disc showed a requirement for the C-terminal transactivation domain of TGO for a cellular response [8].
• Three of the genes, sna, twi, and trh, are known to encode transcription factors and are therefore likely to be part of the network of genes that dictate the malpighian tubule pattern of gene expression [9].
• Another target gene of dysfusion is members only, which inhibits protein nuclear export and influences tracheal fusion. dysfusion also indirectly downregulates protein levels of Trachealess, an important regulator of tracheal development [10].
• Confocal imaging of Single-minded and Trachealess protein localization indicate that they accumulate in cell nuclei when initially synthesized in their respective cell lineages and remain nuclear throughout embryogenesis [11].

Anatomical context of trh

• FKH, in turn, represses trachealess (trh), a duct-specific gene initially expressed throughout the salivary gland primordium. trh encodes a basic helix-loop-helix PAS-domain containing transcription factor that has been proposed to specify the salivary duct fate [12].
• Expression is first induced by exogenous cues and is subsequently autoregulated. trh is also expressed and required in the posterior spiracles and the salivary gland ducts [13].
• Ectopic expression experiments show that Single-minded and Trachealess are localized to nuclei in cells throughout the ectoderm and mesoderm, indicating that nuclear accumulation is not regulated in a cell-specific fashion and unlikely to be ligand dependent [11].
• Using a human probe, two major transcripts (6.1 and 3.1 kb) were identified in mouse and expression was detected in situ in several regions of the mouse brain, including the olfactory bulb, the cerebellum, the cerebral cortex, the pyramidal cell layer of the hippocampus and several hypothalamic nuclei [14].
• At 10 nm indention, the effective transverse stiffness (K( perpendicular)) of myofibrils in rigor solution (ATP-free, pCa 4.5) was 10.3 +/- 5.0 pN nm(-1) (mean +/- SEM, n = 8); in activating solution (pCa 4.5), 5.9 +/- 3.1 pN nm(-1); and in relaxing solution (pCa 8), 4.4 +/- 2.0 pN nm(-1) [15].

Associations of trh with chemical compounds

• 10 g of polypeptide has attached 6.4 g of glucosamine, 3.1 g of galactosamine, 6.1 g of uronic acid, and 2.7 g of neutral sugars [16].
• The degree of inhibition of Ca2+ inflow by primaquine was halved when the extracellular concentration of Ca2+ was increased from 3.1 to 12.5 mM [17].

Physical interactions of trh

• Transcriptional regulation of breathless FGF receptor gene by binding of TRACHEALESS/dARNT heterodimers to three central midline elements in Drosophila developing trachea [18].

Regulatory relationships of trh

• The Drosophila dysfusion basic helix-loop-helix (bHLH)-PAS gene controls tracheal fusion and levels of the trachealess bHLH-PAS protein [7].
• Furthermore, ectopic expression of both Trh and Dfr (but not each one alone) triggered trh autoregulation in several embryonic tissues [19].
• We also determined that the caudal promoter activity can be regulated by Trachealess (Trh)/Tango (Tgo) bHLH-PAS proteins, via the CME sites [20].

Other interactions of trh

• The lineage-specific action of Single-minded and Trachealess derives from transcriptional activation of their genes in their respective lineages, not from extracellular signaling [11].
• We present a model proposing that trachealess is the crucial duct-specific gene that Fork head represses to distinguish pregland from preduct cells [21].
• After the initial establishment of the salivary primordium by Sex combs reduced, fork head excludes eye gone expression from the pregland cells so that its salivary expression is restricted to the posterior preduct cells. trachealess, in contrast, activates eye gone expression in the posterior preduct cells [22].
• On the other hand, the incidence of misrouted axons is significantly increased, most strongly in the trh, twi double mutant [23].
• Applying a combined genetic and biochemical approach has led to the identification of a new protein kinase B/Akt target, the transcription factor Trachealess [24].

Analytical, diagnostic and therapeutic context of trh

• Northern blot analysis revealed the presence of a single Bombyx trh transcript of 5.4 kb [25].
• We analyzed the expression pattern of the Bombyx trh transcript during embryogenesis by in situ hybridization [25].
• Embryonic silk gland development in Bombyx: molecular cloning and expression of the Bombyx trachealess gene [25].

References