Zygotic genome activation (ZGA) is a major genome programming event whereby the 
cells of the embryo begin to adopt specified fates. Experiments in Drosophila 
and zebrafish have revealed that ZGA depends on transcription factors that 
provide large-scale control of gene expression by direct and specific binding to 
gene regulatory sequences. Zelda (Zld) plays such a role in the Drosophila 
embryo, where it has been shown to control the action of patterning signals; 
however, the mechanisms underlying this effect remain largely unclear. A recent 
model proposed that Zld binding sites act as quantitative regulators of the 
spatiotemporal expression of genes activated by Dorsal (Dl), the morphogen that 
patterns the dorsoventral axis. Here we tested this model experimentally, using 
enhancers of brinker (brk) and short gastrulation (sog), both of which are 
directly activated by Dl, but at different concentration thresholds. In 
agreement with the model, we show that there is a clear positive correlation 
between the number of Zld binding sites and the spatial domain of enhancer 
activity. Likewise, the timing of expression could be advanced or delayed. We 
present evidence that Zld facilitates binding of Dl to regulatory DNA, and that 
this is associated with increased chromatin accessibility. Importantly, the 
change in chromatin accessibility is strongly correlated with the change in Zld 
binding, but not Dl. We propose that the ability of genome activators to 
facilitate readout of transcriptional input is key to widespread transcriptional 
induction during ZGA.