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Abstract
Unlike gap genes in the trunk region of Drosophila embryos, gap genes in the head
were presumed not to regulate each other's transcription. Here, we show that in tailless
(tll) loss-of-function mutants the empty spiracles (ems) expression domain in the
head expands, whereas it retracts in tll gain-of-function embryos. We have identified
a 304bp element in the ems-enhancer which is sufficient to drive expression in the
head and brain and which contains two TLL and two BCD binding sites. Transgenic reporter
gene lines containing mutations of the TLL binding sites demonstrate that tll directly
inhibits the expression of ems in the early embryonic head and the protocerebral brain
anlage. These results are the first demonstration of direct transcriptional regulation
between gap genes in the head.