A cryptic START domain regulates deeply conserved transcription factors [RNA-Seq]

However, a newer mechanism discussed for TF divergence is the mechanism of differential usage of shared binding sites. Here, TFs can have largely overlapping binding sites but make independent decisions as to whether gene expression at that site will be affected.

Two members of the CLASS III HOMEODOMAIN LEUCINE ZIPPER (HD-ZIPIII) family of TFs, CORONA (CNA) and PHABULOSA (PHB) use this mechanism as a driver of their functional divergence. This differential regulation is controlled, in part, by their START domains. Here we show that the newly identified disorder-containing START (dSTART) domain also contributes to gene regulatory decisions after binding to shared sites.