A new homeotic mutation in the Drosophila bithorax complex removes a boundary separating two domains of regulation.

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Abstract
The bithorax complex specifies the identity of parasegments 5‐14 of Drosophila. Although nine parasegment‐specific functions, abx/bx, bxd/pbx and iab‐2 to iab‐8,9 have been identified, the whole bithorax complex appears to encode only three classes of proteins, Ubx, abd‐A and Abd‐B. Many observations suggest that the parasegment‐specific functions act as positive cis‐regulatory elements of Ubx, abd‐A and Abd‐B. We report the molecular genetics of a new gain‐of‐function mutation, Fab‐7, which transforms parasegment 11 into parasegment 12. Induction of Abd‐B mutations in cis (one of which removes the Abd‐B homeobox) causes reversion of the dominant phenotype, demonstrating that Fab‐7 misregulates Abd‐B. A 4 kb deletion, 30 kb downstream from the Abd‐B transcription unit, is solely responsible for the Fab‐7 phenotype. We consider that the parasegment‐specific functions lie in DNA domains that are sequentially and independently ‘opened’ along the chromosome. Once a domain is opened, the cis‐regulatory sequences within it can carry out their function. We propose that the Fab‐7 deletion removes a boundary separating the iab‐6 and iab‐7 cis‐regulatory regions (the functions specific for parasegments 11 and 12) allowing the open configuration of iab‐6 to invade iab‐7 in parasegment 11. This is strongly supported by our finding that Fab‐7 can be caused to revert by lesions not only in iab‐7 but also in iab‐6.

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