Figure 2. PQM-1 Is the DAE-Binding Factor (A) Fold enrichment over random expectation of DBE affinity in sequences bound by each of the 46 transcription factors assayed by the modENCODE consortium using ChIP-seq (Niu et al., 2011); the last stage assayed was analyzed. Shown are the 13 most highly enriched factors (p < 10-16 in each case; see Extended Experimental Procedures). As expected, the highest enrichment is found in DAF-16-bound regions. (B) Same as (A), but for DAE affinity. The latter is strikingly enriched within sequences bound by PQM-1. (C) Distribution of ChIP-seq binding site centers relative to transcriptional start sites, based on all modENCODE ChIP-seq data (Niu et al., 2011). (D) PQM-1-binding sites are significantly enriched upstream of both class I and class II genes, with the strongest effect for class II. (E) PQM-1 targets are predicted to primarily be intestinally expressed, and depleted in neurons. (F) Both class I and class II genes are specifically downregulated in the
pqm-1 mutant relative to wild-type. (G-J) A promoter-GFP construct of a PQM-1-regulated class II gene, F55G11.2, that containsa DAE motif in its promoter is abundantly expressed in the intestine of wild type worms, but its expression isdecreased in the
pqm-1(-)background (p<0.0001, Student's t test for unpaired samples), when the DAE is mutated (p<0.001) (H, I, J), and in a
daf-2 background (I and J), and is increased in a
daf-18/PTEN background in a DAE-dependent manner (J). Data are represented as mean +/- SEM (H, I, and J).