The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

age-1  -  Protein AGE-1

Caenorhabditis elegans

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of age-1

  • The role of genetically determined aging pathways in the progression of age-dependent polyQ-mediated aggregation and cellular toxicity was tested by expressing Q82 in the background of age-1 mutant animals that exhibit an extended lifespan [1].
  • In addition, control experiments to determine the amount of RNA contributed by E. coli bacteria (present in the nematode culture medium as a food source) suggest that the age-1 mutant strain has a lower bacterial infection rate, which may contribute to the increased life span of this strain [2].
  • We have shown that mutations in the age-1, and/or age-2 genes of C. elegans, that normally enhance life expectancy, can also increase resistance to killing by the bacterial pathogens Pseudomonas aeruginosa, Salmonella enterica var [3].

High impact information on age-1

  • In Caenorhabditis elegans, mutations that reduce the activity of an insulin-like receptor (daf-2) or a phosphatidylinositol-3-OH kinase (age-1) favour entry into the dauer state during larval development and extend lifespan in adults [4].
  • The gene age-1 is required for non-dauer development and normal senescence. age-1 encodes a homologue of mammalian phosphatidylinositol-3-OH kinase (PI(3)K) catalytic subunits [5].
  • Mutant males also show a lengthening of life and a slowing of the rate of acceleration of mortality, although age-1 mutant males still have significantly shorter life-spans than do hermaphrodites of the same genotype [6].
  • The Itt phenotype cosegregates with age-1 [7].
  • Its position on the physical map of the genome was in the region to which the age-1 gene has been genetically mapped, but it is unlikely that a mutation at the SOD locus confers the Age phenotype [8].

Biological context of age-1

  • Mutations in daf-2 and age-1, which produce a dauer constitutive (Daf-C) phenotype, and in clk-1, which are believed to slow metabolism, markedly increase adult lifespan [9].
  • Mutations in either the daf-2 insulin receptor-like (IRL) gene or the age-1 encoded PI3'K catalytic subunit homolog cause constitutive dauer formation and also affect the life span, brood size, and metabolism of nondauer animals [10].
  • Both daf-2 and age-1 act at a similar point in the genetic epistasis pathway for dauer arrest and longevity and regulate the activity of the daf-16 gene [11].
  • The age-1 strain TJ401 displayed hyperresistance to oxidative stress relative to its parental strain [8].
  • Two recent papers report that daf-2 encodes a member of the insulin-receptor family and that age-1 encodes a PI3 kinase subunit, a second-messenger producing enzyme known to act downstream of the mammalian insulin receptor [12].

Anatomical context of age-1

  • We conclude that increased expression of proteins that protect eukaryotic cells against environmental stress and/or repair stress-induced molecular damage confers hypertonic stress resistance in C. elegans daf-2/age-1 mutants [13].

Associations of age-1 with chemical compounds

  • We found that daily short-term exposure (3 h) to hyperoxia further extended the life span of age-1, a phenomenon known as an adaptive response. age-1 also showed resistance to paraquat and heat [14].
  • Mutations in the daf-2 insulin receptor-like gene or the downstream age-1 phosphoinositide 3-kinase gene extend adult life-span by two- to threefold [15].
  • However, age-1 animals unable to synthesize trehalose survive poorly under hypertonic conditions [13].
  • Here, we quantitatively analyzed total RNA, poly(A)+ RNA, and ribosomal RNA as a function of chronological age in two different strains (TJ1060 and TJ1061) having wild-type life spans and in a long-lived age-1 mutant strain (TJ1062) [2].

Other interactions of age-1

  • These genes include an insulin-like receptor (daf-2) and a phosphatidylinositol 3-OH kinase (age-1) regulating a forkhead transcription factor (daf-16) [6, 7], as well as genes mediating metabolic throughput [8], sensory perception [9], and reproduction [10] [16].
  • Each of three well-studied mutants (age-1, clk-1, and spe-26) alters age-specific mortality rates in a fashion unique to itself [17].
  • Mutations in daf-16 cause a dauer-defective phenotype and are epistatic to the diapause arrest and life span extension phenotypes of daf-2 and age-1 mutants [11].
  • MT1 mRNA levels were significantly (P<0.05) higher in daf-2 mutants compared to age-1 mutants and wild-type C. elegans under basal conditions [18].
  • Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation [19].


  1. The threshold for polyglutamine-expansion protein aggregation and cellular toxicity is dynamic and influenced by aging in Caenorhabditis elegans. Morley, J.F., Brignull, H.R., Weyers, J.J., Morimoto, R.I. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  2. Total RNA, rRNA and poly(A)+RNA abundances during aging in Caenorhabditis elegans. Fabian, T.J., Johnson, T.E. Mech. Ageing Dev. (1995) [Pubmed]
  3. Age influences resistance of Caenorhabditis elegans to killing by pathogenic bacteria. Laws, T.R., Harding, S.V., Smith, M.P., Atkins, T.P., Titball, R.W. FEMS Microbiol. Lett. (2004) [Pubmed]
  4. Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans. Tissenbaum, H.A., Guarente, L. Nature (2001) [Pubmed]
  5. A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans. Morris, J.Z., Tissenbaum, H.A., Ruvkun, G. Nature (1996) [Pubmed]
  6. Increased life-span of age-1 mutants in Caenorhabditis elegans and lower Gompertz rate of aging. Johnson, T.E. Science (1990) [Pubmed]
  7. Thermotolerance and extended life-span conferred by single-gene mutations and induced by thermal stress. Lithgow, G.J., White, T.M., Melov, S., Johnson, T.E. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  8. Aging and resistance to oxidative damage in Caenorhabditis elegans. Larsen, P.L. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  9. A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-C and clk-1 mutants. Taub, J., Lau, J.F., Ma, C., Hahn, J.H., Hoque, R., Rothblatt, J., Chalfie, M. Nature (1999) [Pubmed]
  10. Regulation of the insulin-like developmental pathway of Caenorhabditis elegans by a homolog of the PTEN tumor suppressor gene. Gil, E.B., Malone Link, E., Liu, L.X., Johnson, C.D., Lees, J.A. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  11. An insulin-like signaling pathway affects both longevity and reproduction in Caenorhabditis elegans. Tissenbaum, H.A., Ruvkun, G. Genetics (1998) [Pubmed]
  12. Methuselah meets diabetes. Thomas, J.H., Inoue, T. Bioessays (1998) [Pubmed]
  13. Transcriptional targets of DAF-16 insulin signaling pathway protect C. elegans from extreme hypertonic stress. Lamitina, S.T., Strange, K. Am. J. Physiol., Cell Physiol. (2005) [Pubmed]
  14. Adaptive responses to oxidative damage in three mutants of Caenorhabditis elegans (age-1, mev-1 and daf-16) that affect life span. Yanase, S., Yasuda, K., Ishii, N. Mech. Ageing Dev. (2002) [Pubmed]
  15. Regulation of C. elegans life-span by insulinlike signaling in the nervous system. Wolkow, C.A., Kimura, K.D., Lee, M.S., Ruvkun, G. Science (2000) [Pubmed]
  16. The OLD-1 positive regulator of longevity and stress resistance is under DAF-16 regulation in Caenorhabditis elegans. Murakami, S., Johnson, T.E. Curr. Biol. (2001) [Pubmed]
  17. Longevity genes in the nematode Caenorhabditis elegans also mediate increased resistance to stress and prevent disease. Johnson, T.E., Henderson, S., Murakami, S., de Castro, E., de Castro, S.H., Cypser, J., Rikke, B., Tedesco, P., Link, C. J. Inherit. Metab. Dis. (2002) [Pubmed]
  18. Longevity and heavy metal resistance in daf-2 and age-1 long-lived mutants of Caenorhabditis elegans. Barsyte, D., Lovejoy, D.A., Lithgow, G.J. FASEB J. (2001) [Pubmed]
  19. Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation. Malone, E.A., Inoue, T., Thomas, J.H. Genetics (1996) [Pubmed]
WikiGenes - Universities