ABSTRACTvg w is a homozygous lethal mutation killing embryos prior to formation of the syncitial blastoderm. In heterozygous condition it causes duplications of the posterior wing, ranging from very small duplications of the axillary cord and alar lobe to large duplications including much of the wing blade and the posterior row of bristles. No anterior margin structures are ever observed. The thorax is sometimes slightly abnormal, but rarely shows large duplications. The size of the wing is related to the number of pattern elements deleted or duplicated.Heterozygous vgw flies also show homoeosis of the haltere to wing. This occurs in the capitellum, where wing blade is observed, but no wing margin structures are found. As with the bithorax (bx) mutation which transforms anterior haltere to anterior wing this aspect of the phenotype is repressed by the Contrabithorax (Cbx) mutation. The transformed haltere discs show more growth than wild-type haltere discs.Flies heterozygous for vgw also show a high frequency of pupal lethality, those forming pharate adults generally show the most extreme vgw phenotype.No cell death has been observed in the Imaginal discs of third instar larvae, suggesting that if the wing defects result from cell death this must occur early in development. The homoeosis in the haltere discs and duplications of the wing disc are reflected by the altered morphology and growth of these discs.There are some minor differences in the expressivity of the phenotype when flies are reared at different temperatures. Chromosome substitutions suggested that all aspects of the phenotype related to the vgw mutation and that other mutations had not occurred in the stock. Cytological analysis indicated that vgw is a deletion or inversion on the right arm of chromosome 2 from 47F/48A to 49C.Complementation studies with various mutants thought to be located within the deletion, or inversion and which affect wing morphology have been undertaken.Cbx causes transformations of wing to haltere; this occurs in the posterior compartment far more frequently than in the anterior compartment. Cbx; vgw flies have wings where one of the duplicates is no longer present, presumably transformed to haltere, though this is difficult to identify. One copy of the axillary cord, alar lobe etc, the structures commonly duplicated in vgw, are present, but they are the anterior duplicate rather than the original posterior copy of these structures. Thus Cbx acts upon genuine posterior structures but not those posterior structures in vgw which form in anterior wing locations, suggesting that although these structures differentiate into posterior wing, to the Cbx gene product the cells are still ‘anterior’.