Bicoid functions without its TATA-binding protein-associated factor interaction domains

Four maternal systems are known to pattern the early Drosophila embryo. The key component of the anterior system is the homeodomain protein Bicoid (Bcd). Bcd needs the contribution of another anterior morphogen, Hunchback (Hb), to function properly: Bcd and Hb synergize to organize anterior development. A molecular mechanism for this synergy has been proposed to involve specific interactions of Bcd and Hb with TATA-binding protein-associated factors (TAF(II)s) that are components of the general transcription machinery. Bcd contains three putative activation domains: a glutamine-rich region, which interacts in vitro with TAF(II)110; an alanine-rich domain, which targets TAF(II)60; and a C-terminal acidic region, which has an unknown role. We have generated flies carrying bcd transgenes lacking one or several of these domains to test their function in vivo. Surprisingly, a bcd transgene that lacks all three putative activation domains is able to rescue the bcd(E1) null phenotype to viability. Moreover, the development of these embryos is not affected by the presence of dominant negative mutations in TAF(II)110 or TAF(II)60. This means that the interactions observed in vitro between Bcd and TAF(II)60 or TAF(II)110 aid transcriptional activation but are dispensable for normal development.