The role of the T-box gene optomotor-blind in patterning the Drosophila wing

Abstract

The development of the Drosophila wing is governed by the action of two morphogens encoded by the genes decapentaplegic (dpp; a member of the BMP gene family) and wingless (wg; a member of the WNT gene family), which promote cell proliferation and pattern the wing. Along the anterior/posterior (A/P) axis, the precise expression of decapentaplegic and its receptors is required for the transcriptional regulation of specific target genes. In the present work, we analyze the function of the T-box gene optomotor-blind (omb), a decapentaplegic target gene. The wings of optomotor-blind mutants have two apparently opposite phenotypes: the central wing is severely reduced and shows massive cell death, mainly in the distal-most wing, and the lateral wing shows extra cell proliferation. Here, we present genetic evidence that optomotor-blind is required to establish the graded expression of the decapentaplegic type I receptor encoded by the gene thick veins (tkv) to repress the expression of the gene master of thick veins and also to activate the expression of spalt (sal) and vestigial (vg), two decapentaplegic target genes. optomotor-blind plays a role in wing development downstream of decapentaplegic by controlling the expression of its receptor thick veins and by mediating the activation of target genes required for the correct development of the wing. The lack of optomotor-blind produces massive cell death in its expression domain, which leads to the mis-activation of the Notch pathway and the overproliferation of lateral wing cells.

Muscle Cell Fate Choice Requires the T-Box Transcription Factor Midline in Drosophila

“…Brachyenteron, the ortholog of vertebrate Brachyury, mediates the early specification of the caudal visceral mesoderm (Kusch and Reuter 1999;Hamaguchi et al 2012). Lastly, the Tbx3 ortholog Optomotor-blind (Omb) has been implicated in development of the optic lobe and wing (Grimm and Pflugfelder 1996;Shen et al 2010) and adult abdominal segments (Kopp and Duncan 2002), where it is a downstream target of Decapentaplegic (Dpp) (Haerry et al 1998) and controls proliferation (del Alamo Rodriguez et al 2004;Zhang et al 2013). Future studies will be necessary to determine whether, as with Mid, muscle expression of other T-box proteins has been overlooked and whether, as shown for Mid and Org-1, T-box factors represent a new family involved in the combinatorial control of muscle fate specification.…”

Regulation and function of Spalt proteins during animal development

“…The mechanism of repression by Brinker does not rely on competition with Mad-Medea overlapping sites, but on the existence of adjacent binding sites for Brinker and Mad/Med (Barrio and de Celis, 2004). Additional factors such as the T-box transcription factor Optomotor blind, the trithorax protein Ash2, the activator complex Vestigial/Scalloped and the repressor Groucho are also involved in the regulation of sal in the wing blade (Guss et al, 2001;del Alamo Rodriguez et al, 2004;Angulo et al, 2004;Winter and Campbell, 2004;Hasson et al, 2005). The enhancer regulating salr expression in the wing blade has not yet been identified.…”

Repression of Dpp targets in theDrosophilawing by Brinker

“…A recent study showed that sal expression is dependent upon Omb (del Alamo Rodriguez et al, 2004), suggesting that the lack of ectopic sal expression in lateral brk F138 clones (i.e. outside of the omb domain) could be explained by the absence of ectopic omb in these clones, rather than by Brk F138 directly repressing sal.…”