Gap gene properties of the pair-rule gene runt during Drosophila segmentation

Abstract

The Drosophila Runt protein is a member of a new family of transcriptional regulators that have important roles in processes extending from pattern formation in insect embryos to leukemogenesis in humans. We used ectopic expression to investigate runt's function in the pathway of Drosophila segmentation. Transient over-expression of runt under the control of a Drosophila heat-shock promoter caused stripe-specific defects in the expression patterns of the pair-rule genes hairy and even-skipped but had a more uniform effect on the secondary pair-rule gene fushi tarazu. Surprisingly, the expression of the gap segmentation genes, which are upstream of runt in the segmentation hierarchy was also altered in hs/runt embryos. A subset of these effects were interpreted as due to an antagonistic effect of runt on transcriptional activation by the maternal morphogen bicoid. In support of this, expression of synthetic reporter gene constructs containing oligomerized binding sites for the Bicoid protein was reduced in hs/runt embryos. Finally, genetic experiments demonstrated that regulation of gap gene expression by runt is a normal component of the regulatory program that generates the segmented body pattern of the Drosophila embryo.