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
    lin-14 abnormal cell LINeage 14 A loss-of-function mutation in lin-14 extends lifespan by 31% while a gain-of-function mutation decreases lifespan. The life-extending effects is dependent on daf-16 and hsf-1. Also, lin-14 is a target of lin-4 [16373574]. lin-14(n719) mutation extends mean and maximum lifespan of control animals by 20 and 67%, respectively [23097426]. Knockdown of lin-14 only during adulthood is sufficient to extend lifespan and suppresses the short lifespan phenotype of lin-4 mutants. Nematode
    isp-1 Iron-Sulfur Protein A missense mutation in isp-1 leads to low oxygen consumption, decreased sensitivity to reactive oxygen species, and increased mean (60%) and maximum (100%) lifespan. An isp-1;daf-2 double mutant has a lifespan that is longer than either single mutant, but the lifespan extension of the double mutant is not addative relative to each single mutant [11709184]. Nematode
    aps-1 AdaPtin, Small chain (clathrin associated complex) 1 aps-1 RNAi in the adulthood extends mean lifespan by 8% without any apparent effect on maximum lifespan [23144747]. Nematode
    asb-1 ATP Synthase B homolog asb-1 RNAi in the adulthood extends the mean lifespan by 7% without changing the maximum lifespan [23144747]. Nematode
    rict-1 RICT0r (Rapamycin-Insensitive Companion of TOR) homolog C. elegans with mutations in the TORC2 complex gene rict-1 (Rictor) grow slowly and have small body size, and live slightly longer than wild-type when maintained on “rich” food such as the RNAi feeding strain HT115 and at elevuated temperature (25 degree Celsius) [Soukas et al., 2009 in (Robida-Stubbs et al., 2012)]. rict-1 RNAi at 20 degree Celsius in the adulthood increases mean, median, 75th %ile and maximum lifespan by 12-42, 22-29, 13-32 and 28-54%, respectively, dependent on skn-1. daf-16 is not required for lifespan to be increased by rict-1 RNAi, or when TORC1 and TORC2 are blocked by ragc-1;rict-1 RNAi. rict-1 RNAi extends mean, median, 75th %ile and maximum lifespan in the intestine-specific RNA stains VPS288 by 18, 19, 18 and 16%, respectively [22560223]. Nematode
    C26B2.2 C26B2.2 knockout mutations extend lifespan [15253933]. Nematode
    C47D12.2 TRRAP-like (transcription/transformation domain-associated protein) C47D12.2 RNAi in the adulthood extends mean and maximum lifespan by 6 and 9% [23144747]. Nematode
    cha-1 abnormal CHoline Acetyltransferase 1 cha-1 encodes a choline acetyltransferase which is expressed in motor [18041778] neurons and downregulated in space. Mutation or RNA interference of cha-1 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium [22768380]. cha-1(TY1652) mutation extends mean, 75%ile, and maximum lifespan by 23, 29, and 38%. The cha-1(PR1152) allele extends mean, 75%ile, and maximum lifespan by 22-49, 18-25, and 11-21%. Lifespan extension by cha-1 mutation is not abolished by daf-16 RNAi inactivation. eat-2 RNAi shortens the lifespan of cha-1 mutants. RNAi inactivation of cha-1 reduces Q35 aggregation [22768380]. cha-1 participates in determining pharyngeal pumping rate to affect food intake [6698395]. Nematode
    che-2 abnormal CHEmotaxis che-2 recessive loss-of-function mutations extend lifespan up to 50% (in Bristol N2) [10617200]. che-2 mutants are chemotactic defective, slightly small, defective for osmotic avoidance, have ciliated neurons with abnormal stunted ultrastructure, and are dauer defective [2428682; 1732156]. Nematode
    chn-1 C-term of Hsp70-iNteracting protein (CHIP family) 1 chn-1 RNAi in the adulthood extends mean and maximum lifespan by 7 and 9%, respectively [23144747]. Nematode
    frh-1 FRataxin (involved in human Friedrich's ataxia) Homolog Complete absence of frataxin,the mitochondrial protein defective in individuals with Friedreich ataxia is lethal, while its partial deficiency extends animal lifespan in a p53 dependent manner. Frataxin knockdown via RNAi extends mean and maximum lifespan by 19 and 37%, respectively [23247094]. Substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression. Frataxin expression modulates autophagy in the absence of p53 [23247094]. 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
    daf-1 abnormal DAuer Formation daf-1(mk40) mutation increases mean lifespan by 18-46% and maximum lifespan by 29% [17900898]. The daf-1(m40) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 overexpression, but it results in a temperautre-sensitive, dauer-constitutive phenotype in larvae [11242085]. Nematode
    daf-14 abnormal DAuer Formation daf-14(m77) mutation increases mean lifespan by 21-44% and maximum lifespan by 29% [17900898]. Nematode
    daf-2 abnormal DAuer Formation 2 daf-2 mutants live more than twice as long as controls. daf-2(sa189) mutation extends mean and maximum lifespan by 133 and 129%, respectively, when shifted to 20 degree Celsius. The daf-2(e1370) mutation extends mean and maximum lifespan by 32 and 119%, respectively, when shifted to 25 degree Celsius and by 110 and 145%, respectively, at 20 degree Celsius. daf-2(sa189) mutation extends mean lifespan by 67% as well as maximum lifespan [8247153]. This lifespan extension requires the activity of daf-16 [8247153]. The lifespan extension of daf-2(e1370) mutants is cancelled out by daf-16(m26) mutation. daf-2 mutants still exhibit a long lifespan after ablation of the gonad and germ cells. [8247153]. daf-2(e1370) increases mean (95-118%) and maximum (165%) lifespan [18828672]. RNAi against daf-2 extends mean and maximum lifespan by 47 and 65% [12471266]. daf-2 mutation extends lifespan of wild-type and eat-2 mutants [9789046]. Long lifespan of daf-2 insulin receptor mutation is further extended by sDR. However, daf-2 mutation is not a null mutation, therefore it is still possible that part of sDR-induced increase in lifespan might depend on insulin receptor pathway [17900900]. DR by bacterial dilution extends lifespan of daf-2 mutants [17538612]. IF does not markedly extend lifespan of daf-2 mutants [19079239]. 2% glucose reduce fractions of animals that become dauers at 22.5 degree Celsius in daf-2 mutants. Glucose almost completely suppresses lifespan extension of daf-2 ligand binding domain and tyrosine kinase mutants back to wild-type levels [19883616]. daf-2 mutation increases average lifespan by 157%. Under AL daf-2 mutation increases lifespan by 30%. bDR increases lifespan by 65%. daf-2 mutation further increases lifespan under bDR by 40%. Resistance to oxidative stress is reduced daf-2 mutation [19924292]. daf-2 RNAi increases mean lifesapn by 89% [18828672]. daf-2(m577) mutation increases mean and maximum lifespan by 33 and 29%, respectively, while daf-2(e1370) mutation increases mean and maximum lifespan by 101 and 181%, respectively [16782295]. DR from eat-2(ad465) mutation has an addative effect on lifespan of daf-2(e1370) adults, but not on lifespan of daf-2(e1368) adults [18043747]. Mutation in daf-2 in combination with mutation of daf-12 results in nearly 300% increase in lifespan [7789761]. daf-2 mutants are dauer constitutive [7219552] and exhibit reduced brood size [9504918; 9725835]. daf-2 mutants synergize with germ line ablation for lifespan extension [10360574] and also exhibit synergy with clk-1 mutation for lifespan prolongation [8638122]. All the phenotypes of daf-2 mutants are suppressed by mutation of daf-16 [8247153; 8601482; 7789761; 9725835; 9504918]. Mutation of daf-2 increases expression of sod-3 [10428762]. daf-2(e1370) increases mean lifespan by 146% [23097426]. Reducing expression of daf-2 in the adult stage alone extends lifespan [12399591]. Nematode
    daf-4 abnormal DAuer Formation daf-4(e1374) mutation increases mean and maximum lifespan by 40-120% and 76-83%. daf-4(m63) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 [11242085]. mutation of daf-4 results in a temperature-sensitive, dauer-constitutive phenotype in larvae. sir-2.1 overexpression in the daf-4(m63) background results in an increase in the severity of the dauer-constitutive phenotype [11242085]. Nematode
    daf-7 abnormal DAuer Formation daf-7 mutation does not significantly change lifespan [8247153]. Mutations in daf-7 cause up to 50% mean and maximum life-extension. This effect is dependent upon daf-3 and on daf-16 but independent of daf-2. daf-7(e1372) increases mean and maximum lifespan by 13-39% and 55%, respectively. daf-7(m62) increases mean and maximum lifespan by 20-29% and 29% [17900898]. RNAi against daf-7 only in the adulthood increases mean and maximum lifespan by 26 and 7%, respectively [17900898]. Nematode
    daf-8 abnormal DAuer Formation daf-8 mutation in adults increases mean lifespan by 9-31% but it did not increase maximum lifespan [17900898]. Nematode
    dct-12 DAF-16/FOXO Controlled, germline Tumor affecting 12 dct-12 appears to stimulate the growth of gld-1 tumours. RNA interference of dct-12 increases mean lifespan by 14% in wild-type animals, 16% in daf-16 mutants and 12% in gld-1 mutants [17934462]. Nematode
    dct-13 DAF-16/FOXO Controlled, germline Tumor affecting 13 dct-13 appears to stimulate the growth of gld-1 tumours. RNA interference of dct-13 increases mean lifespan by 23% and maximum lifespan by 20% in wild-type animals. It also increases mean lifespan by 21% in daf-16 mutants and 13% in gld-1 mutants [17934462]. Nematode
    dct-14 DAF-16/FOXO Controlled, germline Tumor affecting 14 dct-14 appears to stimulate the growth of gld-1 tumours. RNA interference increases mean lifespan by 19% in wild-type animals, 21% in daf-16 mutants and 13% in gld-1 mutants [17934462]. Nematode
    dct-15 DAF-16/FOXO Controlled, germline Tumor affecting 15 dct-15 appears to stimulate the growth of gld-1 tumours. RNA interference of dct-15 increases mean lifespan up to 10% in wild-type animals and 9% in gld-1 mutants [17934462]. Nematode
    pept-1 PEPTide transporter family Deletion of pept-1 (alias opt-2 or pep-2) results in retarded development, reduced body size and extended reproductive lifespan. It also further extends (60%) the life-extension caused by daf-2 mutations [15155758]. RNAi of pept-1 increases mean lifespan by 14%. pept-2 is differentially transcribed in daf-16 and daf-2 RNAi animals [12845331]. pept-2 mutants exhibit a decrease in fat content. Nematode
    eat-2 EATing: abnormal pharyngeal pumping EAT-2 eat-2 mutations result in partial starvation by disrupting the function of the pharynx and an approximately 50% extension of lifespan. eat-2 mutants life significant longer by up to 57% [9789046]. eat-2(ad1116) mutants have an extended mean, 75%ile and maximum lifespan by 30, 35, and 24% [22810224]. eat-2 RNAi significantly reduces paralysis in Q35YFP or ABeta42 transgenic animals [18331616]. sDR further increases the long lifespan of eat-2 mutants [19239417]. eat-2 mutants live longer than wild-type at high food concentration but are short lived at lower concentrations (via bacterial dilution) [19229346]. eat-2(ad1113) mutation increases mean lifespan by 56% and is non-additive with SCNA overexpression [16782295]. Combining eat-2 mutation with bacterial deprivation DR does not result in an additive increase in lifespan [17081160;17096674]. Loss of function of eat-2 extends lifespan by 20-30%. Lifespan extension is proposed to be similar to DR. eat-2;daf-2 double mutant live longer than daf-2 single mutants [9789046]. Therefore, eat-2 mutants can synergize with daf-2 mutants, but not with clk-1 mutants, for lifespan extension. Lifespan extension conferred by eat-2 is not suppressed by daf-16 mutation [9789046]. Nematode
    elo-1 fatty acid ELOngation 1 elo-1 RNAi at adulthood extends lifespan by 11%, while in combination with elo-2 (substantial functional redundant) increases lifespan by 15% [21386131]. Nematode
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    • 25 of 269 factors
    Factors are an extension of GenAge and GenDR.

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