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. 2017 May 26;13(5):e1006801. doi: 10.1371/journal.pgen.1006801

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© 2017 Qi et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 5 — (A) Expression of Psod-3::GFP in daf-2 animals is DAF-16, but not SMA-6 dependent. (B) Transcription of candidate target genes of DAF-16 and SMA-2/3 are activated in shc-1;Is[daf-16::GFP] animals. Mutation in either daf-16 or sma-6 suppresses their activation. P-values are summarized in the S8 Table. (C) DAF-16 and SMA-3 binding is enriched in the promoter regions of hpo-11 and rheb-1 genes. Enrichment was determined by ChIP using α-GFP antibody for DAF- 16::GFP or GFP::SMA-3 and normalized to daf-15 3’UTR region that is supposed not to be bound by DAF-16 or SMA-3. Error bars represent the SEM. (D) Transcriptional regulation of the four candidate target genes by DAF-16 in daf-2 mutant animals. P-values are summarized in the S8 Table.