GENETIC-MAPPING OF THE AMIDE RESPONSE ELEMENT(S) OF THE HSR-PI LOCUS OF DROSOPHILA-MELANOGASTER

Small chromosomal deletions [Df(3R)e(R-1) and Df(3R)e(P)] with intact hsr omega transcription units but With variable deletions of the upstr eam region were used to map the upstream regions that regulate heat sh ock and amide responsivity of the 93D puff (hsr omega locus) in saliva ry glands of late third instar larvae of Drosophila melanogaster. The Df(3R)e(P) deletion, generated by a P-element mobilization screen, rem oved the 93B6-7 to 93D3-5 cytogenetic region. [H-3]uridine-labeled tra nscription autoradiograms revealed that normal developmental and heat shock-induced expression of the 93D puff remained unaffected in both t he deficiency chromosomes. However, the amide responsivity of the 93D site was lost on the Df(3R)e(P) homolog while the Df(3R)e(R-1) homolog responded normally to amides. Southern hybridizations with a series o f upstream probes mapped the distal breakpoint of the Df(3R)e(P) delet ion between -22 kb and -23 kb of the hsr omega transcription unit. Sin ce the distal breakpoint of Df(3R)e(R-1) is at about -45 kb upstream o f the hsr omega 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/ar e located in the -22 kb to about -45 kb upstream interval. The Df(3R)e (P) and Df(3R)e(R-1) deletions also abolished dosage compensation at t he 93D locus as well as the effect of beta-alanine levels on its heat shock inducibility.