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pubmed:abstractText |
The steroid hormone ecdysone causes dramatic changes in the genetic programs leading to the pupariation of Drosophila melanogaster, and the Broad-Complex (BR-C) gene is known to play a key role in this process. Previously we showed that BR-C regulates developmental changes in transcription and chromatin structure of the 67B heat shock gene cluster, which contains four small hsp genes. Importantly, the downregulation of the hsp23 gene in the BR-C mutants correlates with the absence of a DNase I-hypersensitive site (DHS) at position -1400. To study the functional importance of the DHS-1400, we have introduced genomic fragments containing a modified hsp23 gene into the Drosophila germ line. Our analysis shows that the ecdysone response element is necessary but not sufficient for full developmental expression of hsp23 in the late third instar and that there is, indeed, another regulatory element, in the vicinity of DHS-1400. We also show that hsp23 developmental expression is not tissue specific. A construct lacking the ecdysone response element is unable to direct normal hsp23 expression in all tissues except the brain. Similarly, brain-specific expression is BR-C independent, although in the other tissues we find different requirements for BR-C genetic functions. The effect of the br mutations is restricted to wing imaginal discs and midgut tissue, while that of 2Bc is restricted to the fat body and Malpighian tubules, and mutations in the rbp group have no effect in any of the tissues studied. Thus, BR-C regulatory action is mediated through different genetic functions in a tissue-specific manner.
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