Abstract
DAF-16 and PQM-1: Partners in longevity
Highlights
Twenty years ago it was discovered that loss of insulin/IGF-1-like signaling (IIS) – such as occurs in daf-2(-) mutants – dramatically extends longevity in the nematode C. elegans via the FOXO transcription factor DAF-16 [1,2,3]
Recent results have made it clear that while DAF-16 is responsible for the activation of Class I genes through the DAF-16 binding element (DBE), it does not interact directly with the upstream promoter regions of Class II genes, leaving the down-regulation of the latter in IIS mutants unexplained [7, 8]
Using GFP translational fusions, we found that the nuclear presence of PQM-1 and DAF-16 is controlled by IIS in opposite ways
Summary
Twenty years ago it was discovered that loss of insulin/IGF-1-like signaling (IIS) – such as occurs in daf-2(-) mutants – dramatically extends longevity in the nematode C. elegans via the FOXO transcription factor DAF-16 [1,2,3]. Recent results have made it clear that while DAF-16 is responsible for the activation of Class I genes through the DAF-16 binding element (DBE), it does not interact directly with the upstream promoter regions of Class II genes, leaving the down-regulation of the latter in IIS mutants unexplained [7, 8]. Using a combination of computational and experimental methods, we discovered that the little-studied transcription factor PQM-1 regulates Class II genes (and Class I to a lesser extent), via the DAF-16 associated element (DAE), a GATA-containing motif previously lacking an identified binding factor [5].
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