Pattern abnormalities induced by ectopic expression of the Drosophila gene hairy are associated with repression of ftz transcription.
The pair-rule segmentation gene hairy (h) is expressed and required in alternate metameres in the early Drosophila embryo. We show that h expression outside these domains, driven by an hsp70 promoter, suppresses the expression of fushi tarazu (ftz). The kinetics of action favor h acting directly as a transcriptional repressor. The resulting pattern defects, and the patterns of en and Ubx activity, can be explained if h acts via ftz and other pair-rule genes in the establishment of stable en domains. We present evidence that ftz is required for the initiation of Ubx transcription, but not for its maintenance.
Ish-Horowicz
D
D
Department of Zoology, University of Oxford, England.
Pinchin
S M
SM
D000818:Animals; D002874:Chromosome Mapping; D004330:Drosophila / Q000033:anatomy & histology / Q000196:embryology / Q000235:genetics*; D004625:Embryo, Nonmammalian / Q000166:cytology; D005796:Genes; D005822:Genetic Vectors; D009154:Mutation; D010641:Phenotype; D010957:Plasmids; D014158:Transcription, Genetic