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DBE affinity is significantly enriched in class I, but not in class II. DAE affinity is also enriched in class I, but even more so in class II gene promoters. We interpret these enrichment patterns as providing strong support for the validity of both our target list and our PSAM representations of DBE and DAE. Our results again indicate that the DBE-binding factor (presumably DAF-16 itself) acts primarily as a transcription activator, whereas the (unknown) factor that binds to the DAE may activate transcription of class II targets Liraglutide in daf-16(?) conditions. A collection of genome-wide in?vivo binding profiles for 46 transcription factors including DAF-16 was recently generated using whole-animal ChIP-seq profiling of C.?elegans at various developmental stages ( Niu et?al., 2011). These data provided us with the opportunity to perform an unbiased search for trans-acting factors whose genomic binding sites were enriched for DBE and DAE affinity, respectively, compared to a matching set of control sequences (see Extended Experimental Procedures). Because we are interested in longevity of adult worms, Oxymatrine we focused on the ChIP-seq data for the latest stage available for each factor. As expected, the transcription factor with the highest DBE enrichment was DAF-16 (almost 2-fold, p value?Verubecestat 2012?and?Zhang et?al., 2013). Our observations pointed to PQM-1 as a candidate trans-acting factor that recognizes the DAE. The genome-wide ChIP-seq profiles for all tested transcription factors (TF) exhibit a strong peak ?150?bp upstream of the transcription start site (Figure?2C), consistent with the expression-based analysis reported in Figure?1F. Accordingly, we assigned a PQM-1-binding site to a gene whenever its center fell between ?700 and?+100?bp relative to the transcription start site. Using this criterion, 2,762 genes were defined as PQM-1 targets. Showing this ��regulon�� in the context of our DAF-16 responsiveness ranking revealed strong enrichment in both class I and class II (Figure?2D and Table S4). Notably, in class II, no fewer than 60% of the 200 top responders have PQM-1 ChIP-seq binding sites in the ?700 to?+100?bp region of their promoters, compared to a genome-wide average of 14%.