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The Drosophila morphogen gradient of Bicoid (Bcd) initiates anterior-posterior (AP) patterning; however, it is poorly understood how its ability to activate a target gene may have an impact on this process. Here we report an F-box protein, Dampened (Dmpd) as a nuclear cofactor of Bcd that can enhance its activating potency. We establish a quantitative platform to specifically investigate two parameters of a Bcd target gene response, expression amplitude and boundary position. We show that embryos lacking Dmpd have a reduced amplitude of Bcd-activated hunchback (hb) expression at a critical time of development. This is because of a reduced Bcd-dependent transcribing probability. This defect is faithfully propagated further downstream of the AP-patterning network to alter the spatial characteristics of even-skipped (eve) stripes. Thus, unlike another Bcd-interacting F-box protein Fate-shifted (Fsd), which controls AP patterning through regulating the Bcd gradient profile, Dmpd achieves its patterning role through regulating the activating potency of Bcd.

Dampened regulates the activating potency of Bicoid and the embryonic patterning outcome in Drosophila