Differential usage of shared binding sites drives functional specialization of an essential family of transcription factors [RNA-seq]
Throughout evolution, the duplication and functional divergence of transcription factors (TFs) has driven cellular and organismal complexity. Mechanisms by which paralogous TFs functionally diverge are thus of broad interest yet remain poorly understood. One well-established mechanism underlying TF divergence is the occupation and regulation of distinct sets of genes. Here we test for new mechanisms using CORONA (CNA) and PHABULOSA (PHB), two representative members of the CLASS III HOMEODOMAIN LEUCINE ZIPPER (HD-ZIPIII) family of plant TFs. CNA and PHB have largely overlapping binding profiles yet each paralog has hundreds of uniquely regulated targets. Regulation of a given gene thus depends on whether its local binding site is considered primed (inactive) or regulated (active) by CNA or PHB. This decision appears to be controlled, at least in part, by their lipid binding START domain, proposing a model in which HD-ZIPIII TFs use information integrated by their START domain to generate paralog-specific transcriptional outcomes at commonly bound genes. Taken together, our study identifies a new mechanism of TF paralog divergence and proposes the ubiquitously distributed START evolutionary module as a driver of functional divergence. Overall design: To investigate genes differentially regulated after indiction of CLASS III HOMEOEDOMAIN LEUCINE ZIPPER (HD-ZIPIII) transcription factors. Sequencing was performed on 3 biological replicates of induced and mock induced genotypes of CORONA (CNA) and PHABULOSA (PHB) as well as chimeric CNA constructs.