TRANSCRIPTIONAL REGULATION OF THE DROSOPHILA HOMEOTIC GENE TEASHIRT BY THE HOMEODOMAIN PROTEIN FUSHI-TARAZU

The Drosophila melanogaster gene teashirt (tsh) is essential for segme nt identity of the embryonic thorax and abdomen. A deletion 3' to the tsh transcription unit causes the loss of Ish early expression in the even-numbered parasegments, and the corresponding larval cuticular pat terns are disrupted. tsh function in the odd-numbered parasegments in these mutants is normal by both criteria. The in vivo activities of ge nomic fragments from the deleted region were tested in transgenic embr yos. A 2.0 kb enhancer from the 3' region acts mainly in the even-numb ered parasegments and is dependent on fushi tarazu (ftz) activity, whi ch encodes a homeodomain protein required for the development of even- numbered parasegments. Ftz protein binds in vitro to four distinct seq uences in a 220 bp sub-fragment; these and neighboring sequences are c onserved in the equivalent enhancer isolated from Drosophila virilis. Tsh protein produced under the control of the 220 bp enhancer partiall y rescues a null tsh mutation, with its strongest effect in the even-n umbered parasegments. Mutation of the Ftz binding sites partially abro gates the capacity for rescue. These results suggest a composite mecha nism for regulation of tsh, with different activators such as fit cont ributing to the overall pattern of expression of this key regulator. ( C) 1997 Elsevier Science Ireland Ltd.