Molecular organization of the vestigial region in Drosophila melanogaster.

Abstract

The vestigial (vg) locus of Drosophila melanogaster is involved in wing margin development. In the absence of a vg+ gene, extensive cell death occurs in third instar imaginal discs which results in a complete loss of adult wing margin structures. P‐element tagging was used to obtain a molecular clone of the vg locus, which led to the molecular characterization of approximately 46 kb of DNA from the region. Deficiency analysis and molecular mapping identified sequences, spanning approximately 20 kb of DNA within the larger region, which are necessary for vg function. The molecular map was oriented with respect to a pre‐existing genetic fine structure map of the locus. The centromere distal limits of the locus were defined by deficiency analyses while the proximal end has not yet been conclusively established. However, three transcripts, that are apparently unrelated to vg, provide circumstantial evidence for the proximal limits of the vg locus. The nature of the molecular lesions for several extant recessive or lethal vg alleles was determined, and these were placed on the vg molecular map. The characterization of the lesions associated with two dominant vg alleles and one complex vg allele imply interesting regulatory mechanisms for this locus. As well, a revertant of a 412 insertion mutant allele was shown to have resulted from a further insertion of a roo element into the 412 element.

Control of Drosophila wing and haltere development by the nuclear vestigial gene product.

“…Wing and haltere structures are eliminated completely, owing to extensive cell death in these regions of the larval imaginal discs. The fly also shows a number of other defects (e.g., erect postscuttellar bristles and reduced size), owing to a requirement for vg function during morphogenesis (Williams and Bell 1988). The regulatory mutant vg 83bez exhibits the same loss of wing and haltere functions ( Fig.…”

“…This would account for the ability of vg 83627 to complement all tested recessive viable vg alleles (Williams et al 1990a), as these alleles are cytologically normal and do not alter the intronic region deleted in vg 83627 (Williams et al 1990a). Several recessive null vg alleles have also been identified, on the basis of the phenotypes of these alleles when in trans to each Cold Spring Harbor Laboratory Press on May 11, 2018 -Published by genesdev.cshlp.org Downloaded from other or in trans to Df(2R)vg B (vgB), a cytologically visible deficiency of the vg locus (Williams and Bell 1988;Williams et al 1990a, b). To test the prediction that chromosome pairing is required for complementation, the wing phenotype of flies containing these alleles in trans to vg 83bez was determined (for the origins and locations of the lesions associated with these alleles, see Materials and methods).…”

“…Furthermore, although the location of sequences required to initially establish vg expression in the embryonic disc primordia have not been identified, genetic evidence indicates that all sequences required for wing development reside within the 16-kb interval, including the vg transcription unit (Fig. 1, coordinates 0 to + 16; Williams and Bell 1988;J. Williams, unpubl.).…”

“…The origins, phenotypes, and molecular biology of Df(2R)vg TM, Df(2R)vg B,vg zgd'~,vg 83~27,vg ~w, and vg 12 are reported in Williams and Bell (1988) and Williams et al (1990a), whereas the analysis of In(2R)vg w and its four revertant alleles (vg wnl-a) is described in Williams et al (1990b). The vg nw and vg 12 alleles are associated with an exonic deletion ( + 13 to + 16} and an exonic insertion ( + 2), respectively (for vg region coordinates, see Fig.…”

“…The vg wn2-4 alleles are vg null derivatives of vg w, which have no vg locus alterations (other than the inversion break). Df(2R)vg ~ is a deletion that includes the entire vg locus (Williams and Bell 1988). Oregon-R flies were used as wild type for all studies.…”