N. Core et al., TRANSCRIPTIONAL REGULATION OF THE DROSOPHILA HOMEOTIC GENE TEASHIRT BY THE HOMEODOMAIN PROTEIN FUSHI-TARAZU, Mechanisms of development, 68(1-2), 1997, pp. 157-172
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.