Factors

We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions. o

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  • Species: + -
  • symbol name observation species
    old-2 Overexpression Longevity Determinant Overexpression of old-2 increases slightly, although statistically significant mean and maximum lifespan by 19 and 44% [9768365]. Nematode
    Y47D3A RNAi against Y47D3A.29 decreases mean and maximum lifespan by 19-26% and 34% [18059442]. Nematode
    tbp-1 TATA-Binding Protein RNAi against tbp-1 decreases mean and maximum lifespan by 15-27% and 21%, respectively [18059442]. Nematode
    mpk-1 MAP Kinase RNAi against F43C1.2B (encoding mpk-1) decreases mean and maximum lifespan by 8-14% and 14%, respectively [18059442]. Nematode
    gsa-1 RNAi against R06A10.2 decreases mean and maximum lifespan by 83-85% and 48%, respectively [18059442]. Nematode
    rpt-1 proteasome Regulatory Particle, ATPase-like 1 rpt-1 RNAi in the adulthood decreases the mean and maximum lifespan by 28 and 50%, respectively [23144747]. Nematode
    pat-3 Paralysed Arrest at Two-fold 3 pat-3 RNAi in the adulthood decreases mean and maximum lifespan by 28% and 50%, respectively [23144747]. Nematode
    dpy-27 DumPY : shorter than wild-type 27 dpy-27 RNAi in the adulthood shortens mean and maximum lifespan by 24 and 25%, respectively [23144747]. Nematode
    snap-1 SNAP (Soluble NSF Attachment Protein) 1 snap-1 RNAi in the adulthood reduces mean and maximum lifespan by 34 and 50%, respectively [23144747]. Nematode
    pcf-11 cleavage and polyadenylation factor homolog 11 pcf-11 RNAi in the adulthood decreases mean and maximum lifespan by 19 and 25% [23144747]. Nematode
    lys-1 LYSozyme lys-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. Overexpression of lys-1 increases mean and maximum lifespan by 5 and 26%, but has no significant effect on median lifespan [22737090]. Nematode
    sptf-3 Specificity Protein Transcription Factor 3 RNAi against sptf-3 decreases mean and maximum lifespan by 20 - 28% and 28%, respectively. sptf-3 RNAi in the adulthood decreases the mean and maximum lifespan by 23 and 37% [23144747]. sptf-3 overexpression extends lifespan [18059442]. Nematode
    rab-5 RAB family 5 rab-5 RNAi in the adulthood reduces mean and maximum lifespan by 38 and 50% [23144747]. Nematode
    rpn-11 proteasome Regulatory Particle, Non-ATPase-like 11 rpn-11 RNAi in the adulthood decreases mean and maximum lifespan by 19 and 25%, respectively [23144747]. Nematode
    cdtl-7 CDc-Two Like 7 RNAi against cdtl-7 starting in the adulthood decreases mean and maximum lifespan by 22 and 25%, respectively [23144747]. Nematode
    snap-29 SNAP (Soluble NSF Attachment Protein) homolog 29 RNAi against snap-29 starting in the adulthood decreases mean and maximum lifespan by 49 and 72%, respectively [23144747]. Nematode
    ubc-18 UBiquitin Conjugating enzyme 18 ubc-18 overexpression is unable to extend lifespan (possibly, UBC-18 is not limiting for WWP-1 function in lifespan). Loss of ubc-18 function by mutation or RNAi reduces lifespan at 25 degree Celsius, but only slightly at 20 degree Celsius. RNAi depletion of ubc-18 completely suppresses increased longevity of eat-2 mutants. RNAi depletion of ubc-18 has no effect on long lifespan of isp-1 or daf-2 mutants. Combined knockdown of wwp-1 and ubc-18 by RNAi does not shorten lifespan any further than RNAi of either single gene. Knockdown of ubc-18 suppresses extended lifespan of wwp-1 overexpression [19553937]. Nematode
    aqp-1 AQuaPorin or aquaglyceroporin related 1 aqp-1 expression changes in response to glucose or glycerol. Similar to daf-16 and hsf-1 mutants, aqp-1 mutants were short-lived, and their short lifespan was not further decreased by glucose. Overexpression of aqp-1::GFP rescues short lifespan of aqp-1 deletion mutants and partially prevented glucose from shortening lifespan. Glucose or glycerol feeding downregulates aqp-1 in wild-type. In daf-16 and/or hsf-1 mutants aqp-1 is repressed and glucose feeding does not significantly affect its expression. aqp-1 mutation does not further decrease the short lifespan of daf-16 and/or hsf-1 mutants. aqp-1 transgene is expressed in pharynx and intestine (which behaves as entire endoderm of animal, including adipose tissues). Dietary glucose does not cause significant differences in levels of glucose or glycerol in wild-type vs. aqp-1 mutants [19883616]. Nematode
    nlp-7 Neuropeptide-Like Protein nlp-7 RNAi or overexpression reduces oxidative stress resistance and shortens lifespan of wild-type under AL. nlp-7 RNAi significantly reduces extended lifespan of eat-2 mutants, but failed to block lifespan extension of age-1 or clk-1 mutants. Lifespan of nlp-7 mutants increases only moderately by sDR [19783783]. nlp-7 expression is induced under DR via the use of a chemically defined axenic medium [17023606] and by sDR [19783783]. Nematode
    cup-4 Coelomocyte UPtake defective 4 cup-4 RNAi or overexpession reduces oxidative stress resistance and shortens lifespan of wild-type under AL. cup-4 RNAi significantly reduces the extended lifespan of eat-2 mutants, but failed to block lifespan extension of age-1 or clk-1 mutants. Lifespan of cup-4 mutants increases only moderately by sDR [19783783]. Nematode
    cbp-1 CBP/p300 homolog 1 bDR and daf-2 mutation induce cbp-1 expression. There is no decrease in cbp-1 expression in whole C. elegans during aging. Overexpression of cbp-1 does not significantly affect lifespan. daf-16 RNAi and cbp-1 RNAi reduce average lifespan under AL to about the same extent. Inhibiting cbp-1 via RNAi by 50%, specifically in adult phase and completely blocks lifespan extension of DD, bDR as well as eat-2, glp-1 and clk-1 mutation, but only partially that of daf-2 mutation and not at all that of cold. cbp-1 RNAi completely blocks the lifespan increase by daf-2 mutation under bDR. cbp-1 RNAi blocks the delay of other age-related pathologies by bDR. cbp-1 RNAi prevents protective effects of bDR and accelerates ABeta42-related pathology. bDR significantly delays onset of paralysis even in presence of cbp-1 RNAi. cbp-1 RNAi specifically in adults completely blocks lifespan extension by three distinct protocols of DR (mutation of eat-2), partly by daf-2 mutation but not of cold and blocks the delay of other age-related pathologies by bDR. cbp-1 RNAi has no effect on lifespan in daf-16 hypomorphic mutants. Combining cbp-1 and daf-16 RNAi in wild-type produces similar lifespan as either alone. Resistance to oxidative stress is strikingly reduced by cbp-1 RNAi and cbp-1 RNAi attenuates the protection against oxidative stress by bDR. cbp-1 RNAi accelerates accumulation of autofluorescence, but has no effect on activity, egg laying, or pharyngeal pumping. cbp-1 RNAi does not block induction of daf-16 or hsf-1 by bDR, but does block the induction of DAF-16 target gene, sod-3, and HSF-1 target gene, sip-1 by bDR. cbp-1 RNAi blocks induction of sod-3 expression by daf-2 RNAi. cbp-1 RNAi does not block the increased Nile Red staining produced by daf-2 mutation, but enhanced Nile Red staining. cbp-1 RNAi blocks the effect of bDR on metabolic gene expression from glycolysis towards beta-oxidation. Drugs that enhance histone acetylation increase lifespan and reduce ABeta42-related pathologies, but these protective effects are completely blocked by cbp-1 RNAi. cbp-1 RNAi decreases H4 Lys 5 acetylation and blocks the extension of lifespan as well as delays the onset of paralysis by ABeta1-42 transgene under AL and bDR by sodium butyrate (NaB) and trichostatin (TSA). cbp-1 RNAi does produce dye-filling defects in all C. elegans amphid neurons (ASI, ADL, ASK, AWB, ASH, and ASJ) [19924292]. Nematode
    dve-1 DVE (Defective proVEntriculus in Drosophila) homolog) 1 dve-1 RNAi attenuates lifespan extension by bDR, but only partially that of daf-2 mutation. dve-1 RNAi attenuates protection against oxidative stress by bDR. dve-1 expression is not induced by bDR [19924292]. Nematode
    phb-1 mitochondrial ProHiBitin complex 1 phb-1 RNAi shortens lifespan of wild-type, aak-2, cep-1 (p53) and jnk-1 mutants, but increases lifespan of daf-2, daf-7, daf-4, daf-11, gas-1, mev-1, isp-1, clk-1, nhr-49, fat-7 and gld-1 mutants. daf-16 mutation fully suppressed the exceptional long-lifespan of prohibitin-depleted (via RNAi) daf-2 mutants [19812672]. Nematode
    phb-2 mitochondrial ProHiBitin complex 2 phb-2 RNAi shortens lifespan of wild type, aak-2, cep-1 (p53) and jnk-1 mutants, but increases lifespan of daf-2, daf-7, daf-4, daf-11, gas-1, mev-1, isp-1, clk-1, nhr-49, fat-7, gld-1 mutants. daf-16 mutation fully suppressed exceptionally long-lifespan of via RNAi prohibitin-depleted, daf-2 mutants [19812672]. Nematode
    faah-1 Fatty Acid Amide Hydrolase 1 faah-1 overexpression reduces eicosapentaenoyl ethanolamide (EPEA), palmitoleyol ethanolamide, linoleyol ethanolamide, as well as arachidonoyl ethanolamide (AEA) levels, delays development, increases thermal stress resistance, and was associated with mean and maximum adult lifespan extension by 19 and 35%, respectively, in presence of abundant food but not under (two different protocols of) DR. Overexpression in pharynx was largely sufficient for this lifespan extension [21562563]. Nematode
    Factors are an extension of GenAge and GenDR.

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