Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans

By Coleen T. Murphy, Steven A. McCarroll, Cori Bargmann, Andrew G. Fraser, R. Kamath, J. Ahringer, Hao Li, C. Kenyon. Nature, 2003

2,285 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/74b672c43ef0c9fda37a9812a2e566aead80a72b

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Citations in the corpus

Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans (2007, background): “Moreover, DAF-16 regulates many stress-response genes (Honda & Honda, 1999; McElwee et al., 2003; Murphy et al., 2003) and DAF-16 is known to be activated by environmental stress (Henderson & Johnson, 2001; Lin et al., 2001).”
Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans (2010, background): “Inherent Protein Aggregation Is Modulated by the Insulin/IGF-1 Signaling Pathway Reducing insulin/IGF-1 signaling is known to trigger the expression of many cell-protective proteins and processes [69,70,71,72] that prevent the collapse of proteostasis.”
The plasticity of aging: insights from long-lived mutants. (2005, methodology): “DAF-16 is known to inhibit expression of the insulin-like gene ins-7, a putative DAF-2 agonist (Murphy et al., 2003), and reduced insulin levels could potentially mediate this effect.”
Trends in oxidative aging theories. (2007, background): “Data from the dauer mutants (the best known being mutant daf-2) are generally supportive with the oxidative hypothesis, in that resistance to oxidative stress is consistently elevated in dauer mutants and antioxidant enzymes (most dramatically, MnSOD) are upregulated [67] [68] [69].”
An AMPK-FOXO pathway mediates longevity induced by a novel method of dietary restriction in C. elegans. (2007, background): “AMPK Activates FOXO/DAF-16-Dependent Transcription To gain insight into the mechanism of AMPK’s action on FOXO/DAF-16 transcription factor, we examined the effect of AMPK activity on the expression of sod-3, a known DAF-16 target gene involved in both stress resistance and longevity [20, 32].”
TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO (2012, background): “IIS, TORC1, and TORC2 are each involved in growth, and SKN-1 and DAF-16 functions include maintenance of protein homeostasis and resistance to various stresses (Kenyon , 2010; Lee et al., 2003; Li et al., 2011; McElwee et al., 2007; Murphy et al., 2003; Oliveira et al., 2009).”
The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism and life span (2004, methodology): “We examined 1.8 kb of sequence 5′ of the daf-15 ATG translation initiation site, as well as the first intron for possible DAF-16 binding sites, TTGTTTAC (Lee et al., 2003; Murphy et al., 2003), and for insulin response sequences (IRS) (O’Brien et al., 2001).”
p38 MAPK Regulates Expression of Immune Response Genes and Contributes to Longevity in C. elegans (2006, background): “regulated by DAF-16 [13] and by starvation [27].”
Regulation of longevity in Caenorhabditis elegans by heat shock factor and molecular chaperones. (2003, background): “Elevated expression of multiple heat shock genes (including hsp-16 and Hsp90) has been observed in long-lived daf-2 and age-1 mutants (Hsu et al., 2003; McElwee et al., 2003; Murphy et al., 2003).”
A conserved MST-FOXO signaling pathway mediates oxidative-stress responses and extends life span. (2006, positive): “Consistent with these results, antioxidant and other stress-response genes constitute a prominent set of DAF-16-regulated genes (Lee et al., 2003a; McElwee et al., 2004; Murphy et al., 2003).”