FIGURE 3.

Rhomboid-A (RhoA) and Distal-less conserved regulatory element (DCRE) are regulated through tissue specific co-activators and co-repressors to mediate distinct transcriptional outputs. (A) A simplistic general model for how a Hox CRM yields cell-specific outputs via the direct integration of a Hox factor with the common co-factors Exd and Hth, and a tissue specific TF to mediate either activation or repression (B) In sensory cells, Abd-A, Exd, Hth, and Pax2 interact together to activate gene expression by forming complexes on the RhoA CRM. (C) In the anterior abdomen, Abd-A/Exd/Hth complexes bind together with dFoxG to repress the DCRE CRM. (D) Replacing two of the Hox binding sites from the DCRE with the Abd-A/Hth/Exd sites that mediate activation via the RhoA CRM did not alter the transcriptional response of the DCRE. These data show that the configuration of Hox binding sites does not dictate gene activation versus repression. Instead, it is the presence of nearby dFoxG sites [repression in (D)] or Pax2 sites [activation in (B)] that dictates transcriptional outcomes. (E) In the posterior abdomen, En interacts with Abd-A and Exd/Hth to repress the DCRE CRM. (F) In the thorax ectoderm, the Antp Hox factor cooperatively binds with Exd to stimulate gene expression. This activation activity does not require the dFoxG nor the En sites. In this model, we propose that an unknown tissue specific TF mediates activation of DCRE CRM to result in ectoderm specific gene activation.