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Symbol: Ara Flybase ID: FBgn0015904
Synonyms: {Name} {GadFly}
Function: {Short_Function} {LocusLink}
Keywords: {Keywords} {Interactive_Fly}

  • a member of the iroquois complex (Iro-C)
  • the genes of the Iroquois complex (Iro-C) araucan (ara), caupolican (caup), and mirror (mirr), which encode highly related homeodomain proteins that are members of the prepattern that controls proneural and provein genes (Go´mez-Skarmeta et al. 1996; McNeill et al. 1997), are candidates to perform a basic function in the formation of the notum. Their earliest expression in the wing disc is restricted to the notum territory, and their absence in clones of cells induces malformations in the notum but only relatively minor defects in the patterning of the wing (Go´mez-Skarmeta et al. 1996; Leyns et al. 1996).
  • specification of L3 vein depends on activity of the homeobox-containing genes araucan (ara) and caupolican (cau) from the iroquois complex (iro-C) (Gomez-Skarmeta et al., 1996; Gomez-Skarmeta and Modolell, 1996).
Genetic interactions
  • Flybase list of genetic interactions
  • In vn mutants, expression of Caup/Ara is lost (Fig. 2E) and loss of EGFR signaling, in EGFRts clones, in the medial notum resulted in a loss of Caup/Ara expression (Fig. 2G). However, clones in the lateral notum continued to express Caup/Ara (Fig. 2G), suggesting other factors regulate Iro-C gene expression in these cells at this stage (Wang, 2000)
  • ara and caup expression located at the AP compartment border are necessary for activation of rho at the presumptive vein L3 and of ac-sc at the proneural clusters that will give rise to the sensilla campaniformia associated with vein L3 (Gomez-Skarmeta, 1996)
Physical interactions
{Physical interactions}
Transcriptional Regulation
Location (protein and transcript)
  • ara and caup are expressed ini two symmetric domains separated by the DV boundary and located near or at the AP compartment border (Gomez-Skarmeta, 1996; Leyns, 1996)
  • Caup/Ara are expressed in the presumptive notum at the end of the second instar (Gomez-Skarmeta, 1996; Diez del Corral, 1999) and in a domain that overlaps with vn in early third instar wing discs (Fig 2D) (Wang, 2000)
  • In wild-type discs, ara and col expression partly overlapped, with ara expression extending anteriorly by about three rows of cells into the region corresponding to presumptive L3 vein (Fig. 4I). (Crozatier, 2002)
Protein Modifications and Regulation
Related to
{Related to}
  • Cells lacking Ara or Caup proteins form wing hinge structures (tegula and axillary sclerites) instead of notum. Moreover, the mutant cells impose on neighboring wild-type cells more distal developmental fates, like lateral notum or wing hinge. These findings support a tergal phylogenetic origin for the most proximal part of the wing and provide evidence for a novel pattern organizing center at the border between the apposed notum (Iro-C-expressing) and hinge (Iro-C-nonexpressing) cells. This border is not a cell lineage restriction boundary. (Diez del Corral, 1999)
  • At the notum, clones homozygous for the Iro-C deletions Df(3L)iroDFM1 or Df(3L)iroDFM3 and induced during the first and second larval instars associated with extensive malformations: The notum cuticle was replaced by a mostly naked, corrugated cuticle with sclerotized structures. In 52 of 116 cases [Df(3L)iroDFM3 clones], these structures were clearly identifiable as components of an ectopic wing hinge, for example, axillary sclerites (Fig. 1A,E) and tegula-like cuticle, with characteristic bristles and sensilla trichoidea and campaniformia (Fig. 1B,E). (Diez del Corral, 1999)
    • 43 of the 52 malformations affected the lateral notum. The ectopic axillary sclerites were always arranged in a mirror-image disposition with respect to the extant ones (Fig. 1E). (Diez del Corral, 1999)
    • Malformations at more medial regions of the notum, which did not affect the lateral notum, most frequently contained disorganized groups of tegula-like sensila trichoidea and campaniformia (7 of the 52 malformations; data not shown) and, in 2 cases, almost complete ectopic tegulae (Fig. 1C,D). (Diez del Corral, 1999)
    • Malformations reaching the central-most regions of the notum caused defects in the fusion of heminota, which were separated by an undefined cuticle (not shown). (Diez del Corral, 1999)
    • Clones not associated with malformations appeared in flies irradiated 96–120 hr after egg laying (AEL). They developed normally in the central notum or induced invaginating cuticle vesicles in the lateral regions (not shown). (Diez del Corral, 1999)
  • Iro-C- clones within the notum territory induced a fold around themselves similar to the fold separating notum and wing hinge territories (Fig. 2A). (Diez del Corral, 1999)
    • Moreover, appropriately positioned clones rerouted the notum–hinge fold, and this became continuous with the clone-induced fold (Fig. 2D–F). In contrast, the border of clones contacting hinge cells did not form a fold and had normal, wiggly outlines (Fig. 2E). (Diez del Corral, 1999)
  • The enhancer trap line l(2)09261, a hinge and wing marker that is expressed only weakly in the prospective notum (Figs. 3A,B and 4C), was strongly derepressed in notum Iro-C- cells (Fig. 3C–E). teashirt (tsh), a gene strongly expressed in the hinge and the lateral-most part of the prospective notum, but weakly expressed in the more central parts of the notum (Fig. 3F), was also similarly derepressed in the centrally located Iro-C- clones (Fig. 3G). In contrast, vg, optomotor blind and nubbin (nub), genes that are expressed primarily in the wing and minimally or not expressed in the hinge (Fig. 4A,B; Williams et al. 1991; Ng et al. 1995; Grimm and Pflugfelder 1996), were not expressed in the notum clones (not shown), consistent with the transformation of Iro-C- cells toward a wing hinge identity. (Diez del Corral, 1999)
  • Iro-C- cells affected the surrounding wild-type tissue. (Diez del Corral, 1999)
    • mutant cells that differentiated as ectopic tegula recruited wild-type cells to form part of this ectopic structure (Fig. 1D). This evidenced a change of fate of the wild-type cells from notum to tegula. (Diez del Corral, 1999)
    • the Iro-C- clones in the notum territory induced neighboring wild-type cells to express strongly the l(2)09261 marker (Fig. 3C,E). Interestingly, the expressing cells were located nearest to the notopleural (NP) region; consequently, their spatial disposition with respect to the clone was a mirror-image correlate of the NP cells expressing the marker with respect to the notum/hinge fold (Fig. 3C). This nonautonomous effect was weaker in more posterior clones and was not observed in the postnotum territory (not shown). (Diez del Corral, 1999)
    • A nonautonomous derepression of tsh also occurred in the wild-type cells nearest the lateral notum (Fig. 3G). (Diez del Corral, 1999)
    • Another nonautonomous effect concerned the expression of wg, whose product accumulates in an A/P band that runs near the dorsocentral region of the prospective notum (Baker 1988; Phillips and Whittle 1993) but not in the hinge (except for a small domain at the prospective tegula, Fig. 3H). The Iro-C- cells in the notum, which did not express wg autonomously (Fig. 3I) (in accordance with their transformation toward hinge cells), caused their wild-type neighbors closest to the NP region also not to accumulate Wg protein (Fig. 3J). The nonautonomous repression of wg and activation of l(2)09261 and tsh are consistent with the transformation of these cells toward NP or other lateral notum cells. (Diez del Corral, 1999)
    • Interactions between the Iro-C- and Iro-C+ cells were also revealed by the ectopic fold that surrounded the notum Iro-C- clones (Fig. 2A), as this fold was formed by mutant and wild-type cells (not shown). Moreover, similar interactions evidently occurred at borders where cells with ectopic high levels of Iro proteins confronted cells without or with minimal levels of them, as ectopic folds also formed at these borders (Fig. 2B,C). Therefore, the fold separating the prospective notum and wing hinge (Figs. 2A and 3A,B) is probably induced in early third instar discs by the juxtaposition of Iro-C expressing and nonexpressing cells (Fig. 5B). Other folds or grooves may be similarly induced, as mirr is expressed in the Drosophila embryo, at the dorsal folds, and at the anterior border of each segment (McNeill et al. 1997). Interestingly, the Xiro1 and Xiro2 genes, Xenopus homologs of ara and caup (Go´mez-Skarmeta et al. 1998), are expressed at rhombomeres 1, 3, and 5 and may be involved in generating their borders (J.L. Go´mez-Skarmeta, unpubl.). (Diez del Corral, 1999)
Overexpression / Ectopic expression
  • misexpression of ara cause loss of the wing and duplication of notum (Fig 2A,B) (Wang, 2000)
  • ectopic expression imposes a notum fate on nonnotum cells. (Diez del Corral, 1999)
    • UAS–ara, driven in the dorsal compartment by ap–GAL4 removed the dorsal hinge territory, as defined by the expression of l(2)09261 and the nonexpression of nub (Fig. 4C,D). The resulting pharate individuals lacked all dorsal hinge elements (axillary sclerites and tegula), had strongly reduced and distorted wings, but ectopic notum structures were not discerned (not shown). Similar adult phenotypes were observed with UAS–caup or UAS–mirr transgenes (Go´mez-Skarmeta et al. 1996; McNeill et al. 1997), and phenotypes consistent with these were also found by using drivers dppdisk1-GAL4 (Staehling-Hampton et al. 1994) or Gal4 line C-765 (Go´mez-Skarmeta et al. 1996). Simultaneous expression of UAS–mirr and either UAS–ara or UAS–caup did not modify the results. Moreover, imaginal disc cells strongly overexpressing UAS–caup at the wing pouch still expressed vg or nub (not shown). These results indicate that the Iro proteins cannot impose a notum fate on every wing disc cell, although, if present, they prevent the normal development of the wing hinge. (Diez del Corral, 1999)


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