High impact information on tkv

• Spatially restricted activation of the SAX receptor by SCW modulates DPP/TKV signaling in Drosophila dorsal-ventral patterning [1].
• We propose that spatial regulation of the SAX pathway modulates TKV signaling to create positional information over the embryonic ectoderm [1].
• Ubiquitous expression of a tkv transgene rescues both tkv and sax loss-of-function mutations [2].
• Analysis of clones mutant for the Dpp receptors encoded by punt or thickveins (tkv) reveals that repression of wg expression is one critical function of Dpp signalling in leg and wing discs [3].
• At this stage in development, thickveins, a dpp receptor, is expressed in the mesoderm, and this suggests that ectodermal dpp might not only be required for development of dorsal ectoderm, but could also act inductively to mediate pattern formation in the underlying mesoderm [4].

Biological context of tkv

• To identify components involved in dpp signaling, we carried out a genetic screen for dominant enhancer mutations of a hypomorphic allele of thick veins (tkv), a type I receptor for dpp [5].
• The Tkv downregulation depends on BMP signaling and may provide a positive feedback by allowing the spread of Dpp [6].
• Mutations in punt produce phenotypes similar to those exhibited by tkv, sax, and dpp mutants [7].
• The tkv receptor is therefore involved in delimiting the expression domains of homeotic genes in the visceral mesoderm [8].
• These results indicate a role for D-MEF2 in the regulation of tkv gene expression and Decapentaplegic signal transduction that are essential for proper determination and/or differentiation of the anterior follicle cells [9].

Anatomical context of tkv

• We show that salivary gland posterior migration requires the activities of genes that position the visceral mesoderm precursors, such as heartless, thickveins, and tinman, but does not require a differentiated visceral mesoderm [10].

Physical interactions of tkv

• Brk25D binds dpp protein and bone morphogenetic protein 2 with high affinity [11].

Regulatory relationships of tkv

• smoothened and thickveins regulate Moleskin/Importin 7-mediated MAP kinase signaling in the developing Drosophila eye [12].
• We present evidence that Dpp signaling negatively regulates tkv expression and that the level of receptor influences the effective range of the Dpp gradient [13].

Other interactions of tkv

• mtv shapes the activity gradient of the Dpp morphogen through regulation of thickveins [14].
• During larval development, the expression of spalt, a dpp target, was abolished in mutant wing discs, while it was restored by a constitutively activated form of Tkv (Tkv(Q253D)) [15].
• In this report, we demonstrate that mtv integrates the activities of En and Hh that shape tkv expression pattern [14].
• We suggest that regulation of tkv by HH is a key part of the mechanism that controls the level and distribution of DPP [16].
• The type I receptor Thick veins (Tkv) and the R-Smad transcription factor Mothers-against-dpp (Mad) are localized postsynaptically in the muscle [17].

Analytical, diagnostic and therapeutic context of tkv

• CONCLUSIONS: Our genomic-wide microarray analysis has revealed common targets for the tkv and babo pathways and provided new insights into downstream effectors of two distinct TGFbeta like pathways [18].

References