Abstract
The decapentaplegic gene complex (2-4.0) in Drosophila melanogaster is defined by a series of allelic mutations affecting imaginal disk development. Decapentaplegic (dpp) mutant individuals exhibit a variety of pattern deficiencies and duplications in structures derived from one or more of the 15 major imaginal disks. Based on dpp mutant phenotypes, we suggest that the dpp gene complex is involved in the elaboration of positional information within developing epidermal tissue. The dpp mutations are recessive and fall into six phenotypic classes. Milder alleles (classes I and II) affect only one or a few disks while most alleles (classes III, IV, V and EL) affect all major imaginal disks. Class EL homozygotes are embryonic lethals; development is arrested before germ-band shortening late in gastrulation. Presently inseparable from EL, is a haplo-insufficient function (Hin-d) associated with the distal (left) end of the dpp gene complex. The dpp gene complex occupies most or all of 22F1--3, three densely staining polytene chromosome bands. A colinearity exists between map positions of the four identified functional units within the complex and the severities of mutant phenotypes caused by disruption of these functions. Most dpp mutations are gross chromosomal rearrangements; they exert polar effects on the decapentaplegic functions that are proximal to the rearrangement breakpoints in 22F. Many structural similarities exist between the decapentaplegic and bithorax gene complexes.
