Genetic mapping of the amide response element(s) of the hsr omega locus of Drosophila melanogaster.

Small chromosomal deletions [Df(3R)eR-1 and Df(3R)eP] with intact hsromega transcription units but with variable deletions of the upstream region were used to map the upstream regions that regulate heat shock and amide responsivity of the 93D puff (hsromega locus) in salivary glands of late third instar larvae of Drosophila melanogaster. The Df(3R)eP deletion, generated by a P-element mobilization screen, removed the 93B6-7 to 93D3-5 cytogenetic region. [3H]uridine-labeled transcription autoradiograms revealed that normal developmental and heat shock-induced expression of the 93D puff remained unaffected in both the deficiency chromosomes. However, the amide responsivity of the 93D site was lost on the Df(3R)eP homolog while the Df(3R)eR-1 homolog responded normally to amides. Southern hybridizations with a series of upstream probes mapped the distal breakpoint of the Df(3R)eP deletion between -22 kb and -23 kb of the hsromega transcription unit. Since the distal breakpoint of Df(3R)eR-1 is at about -45 kb upstream of the hsromega gene it is inferred that the amide response element(s) that modulate the specific transcriptional activation of the 93D puff following treatment of salivary glands with a variety of amides is/are located in the -22 kb to about -45 kb upstream interval. The Df(3R)eP and Df(3R)eR-1 deletions also abolished dosage compensation at the 93D locus as well as the effect of beta-alanine levels on its heat shock inducibility.