| VMA2 deletion | VMA2 deletion mutants have a reduced ΔΨ and mitochondrial morphology similar to aged cells. The restoration of the vacuolar acidity in daughter cells requires V-ATPase activity as it is eliminated in VMA2 deletion mutant cells [23172144]. VMA2 deletion mutation decreases the mean replicative lifespan by 80% in the alpha strain [18340043]. Deletion of VMA2 decreases mean, median and maximum replicative lifespan by 84%, 84% and 70%, respectively. DR (0.5% glucose restriction) does not extend the replicative lifespan of VMA2 and shortens it even more [23172144]. | Yeast | -80 to -83.9 | -84.1 | -70.0 |
| KSS1 deletion | Deletion of KSS1 results in increased sensitivity to heat shock and oxidative stress and a 25% reduction in median chronological lifespan [17662940]. | Yeast | — | -25 | — |
| AVT1 deletion | Deletion of AVT1 accelerates the development of age-induced mitochondrial dysfunction without effecting the kinetics of vacuolar acidity decline and prevents the suppression of mitochondrial dysfunction by VMA1 and VPH2 overexpression without affecting vacuolar acidity. AVT1 deletion decreases mean, median and maximum lifespan by 21, 22, and 12%, respectively [23172144]. | Yeast | -20.6 | -22.4 | -11.8 |
| HAC1 deletion | Deletion of HAC1 decreases mean, median and maximum replicative lifespan by 10, 8 and 5%, respectively [23167605]. | Yeast | +10.3 | +8.3 | +5.3 |
| RPS6B deletion | RPS6B deletion increases mean replicative lifespan by about 30% [16293764]. Deletion of RPS6B, but not of the RPS6A paralog increases replicative median lifespan robustly by 45% [17174052]. | Yeast | +30 | +45 | — |
| CYR1 mutation | The CDC35-1 allele of the adenylate cyclase CYR1 confers a 75% extension of replicative lifespan at 25 degree Celsius [11000115]. cyr1-1 mutation extends median chronological lifespan by 28-47% and is non-addative with lifespan extension conferred by overxpression of human MAPK1 [17662940]. | Yeast | +75 | +28 to 47 | — |
| HSP12 deletion | HSP12 deletion slightly increases mean, medium, and maximum replicative lifespan by 24, 27, and 3% under AL, but totally abolishes the lifespan extending effect of moderate DR [Alan Morgan, personal communication; Herbert et al. in press].
HSP12 deletion has no effect on resistance to variety of stresses (including oxidative stress) [Alan Morgan, personal communication]. | Yeast | +24 | +27 | +3 |
| RPL10 deletion | Heterozygosity for RPL10 deletion increases median replicative lifespan by 24% [17174052]. | Yeast | — | +24 | — |
| IDH2 deletion | Deletion of IDH2 increases the mean replicative lifespan by about 30% [16293764]. IDH2 deletion extends mean replicative lifespan by 20% in the alpha strain and in a strain [19030232; 18340043]. IDH2 deletion extends mean, median and maximum lifespan by 15, 19 and 15% [23167605]. | Yeast | +15.4 to +30 | +19.2 | +15.4 |
| TOR1 Deletion | TOR1 deletion extends mean and maximum replicative lifespan by 21 and 25% [16293764] as well as chronological lifespan [21076178]. This lifespan extension is independent of SIR2 and additive with deletion of FOB1 [16293764]. Deletion of TOR1 fails to increase the replicative lifespan of a sir2 mutant [20947565]. Deletion of TOR1 substantially extends chronological lifespan, increasing median survival almost 3-fold (wild-type 4.5 days, tor1 null 12 days), i.e. by 167%. By 21 days in culture, the vast majority of wild-type cells had died (>99.9%), whereas many tor1 null cells remained viable. Deletion of TOR1 also extends the chronological lifespan of the relatively short-lived BY4742 strain, one of the two haploid genetic backgrounds of the widely used Yeast Knockout Collection available from Open Biosystems. Deletion of TOR1 fails to extend chronological lifespan in Petite strains that are unable to respire [17403371]. TOR1 deletion increases replicative lifespan by 30% in the alpha strain and 20% in a strain [19030232]. TOR1 deletion mutant have and increased mean and maximum replicative lifespan by 21% and 6%, respectively [21931558]. Deletion of TOR1 extends replicative lifespan as well as chronological lifespan [21076178] and glucose restriction fails to further extend the long replicative lifespan of tor1Delta [16293764; 16418483; 18225956]. Water starvation (extreme DR) further extends chronological lifespan of tor1 mutants [18225956]. | Yeast | +21 to +30 | +167 | +6 to +25 |
| TMA19 deletion | Deletion of TMA19 increases median replicative lifespan by 16% (P<0.02) [16806052]. TMA19 deletion increases mean replicative lifespan by 25-30% in the alpha and a strains [19030232]. | Yeast | +25 to +30 | +16 | — |
| PHB1 deletion | Deletion of PHB1 results in a slight reduction in mean and maximum replicative lifespan and a defect in mitochondrial membrane potential. When both PHB1 and PHB2 genes are deleted, the mean replicative lifespan is reduced by one third (30%) that of the wild-type strain [9259555]. Deletion of PHB1 decreases replicative lifespan by 20% [12882345]. Phenotypic changes characteristic of aging cells (e.g. lengthening of cell cycle and specific morphological changes) suggests that PHB1;PHB2 double mutants undergo premature aging, not simply reduction of viability [9259555].
There is no reduction in stress resistance or bulk growth rate in PHB1 mutants. PHB1;PHB2 double mutant have a strong defect in mitochondrial potential, while PHB1 mutant have only a slight defect [9259555]. PHB1 deletion is synthetical lethal with mutation of outer mitochondrial membrane proteins, Mdm12, Mdm10, or Mmm1 [9632789]. | Yeast | -30 | — | — |
| PHB2 deletion | PHB2 deletion leads to a slight reduction in both mean and maximum replicative lifespan, and when both PHB1 and PHB2 genes are deleted, the mean replicative lifespan is reduced by 40% [9259555]. Deletion of PHB2 decreases replicative lifespan by 30% [12882345]. Phenotypic changes characteristic of aging cells (e.g. lengthening of cell cycle and specific morphological changes) suggests that PHB1;PHB2 double mutants undergo premature aging, not simply reduction of viability [9259555].
PHB2 mutants exhibit no reduction in stress resistance or bulk growth rate. PHB1;PHB2 double mutant have a strong defect in mitochondrial potential [9259555].
Prohibitin-dependent mutation pbd1 and pdb2 behave in a different manner and probaly affect different aspects of prohibitin function. pdb1 mutants slightly extended lifespan by 11%, whereas in contrast, the pdb2 mutation results in a shortening in both the mean- and the maximum-lifespan (by 28 and 17%, respectively). pdb1 mutation also reduces chronological lifespan. Reducing the expression of the PHB2 in the pbd mutants retards the rate of growth and affects replicative lifespan [16710639]. | Yeast | -30 | — | — |
| PNC1 deletion | Deletion of PNC1 shortens replicative lifespan approximately by 10% [12736687] and largely prevents replicative lifespan extension of 0.5% glucose restriction. 0.5% glucose restriction slightly extends median replicative lifespan (by 10 - 15%) but not maximum replicative lifespan in pnc1Delta [14724176]. PNC1 deletion decreases chronological lifespan [17110466]. | Yeast | -10 | — | — |
| POL1 deletion | Mutation of POL1 results in a 20-60% reduction in mean lifespan (in SS111) [12024027] | Yeast | -20 to -60 | — | — |
| HST1 deletion | Deletion of HST1 blocks the residual replicative lifespan extension by hxk2 mutant in a sir2;fob1;hst2 triple mutant background [16051752]. However, DR can increases the replicative lifespan to a similar extent in sir2;fob1;hst1;hst2 quadruple mutant cells as in sir2;fob1 double mutant cells under 0.5, 0.05 and 0.005% glucose conditions and even by hxk2 deletion mutant [16741098; 17129213]. | Yeast | — | — | — |
| PUF4 deletion | Deletion of PUF4 has no effect on replicative lifespan in either uth4-14c (C-terminal truncation) or UTH4 background. However, PUF4 is required for lifespan extension by the semi-dominant Sir4-42 allele in the uth4-14c background [9150138].
PUF4 is required for nucleolar relocalization of Sir3 in a Sir4-42 background [9150138]. puf4;mpt5 double deletion strain has increased telomere silencing reltive to the mpt5 single mutant [9651685]. | Yeast | — | — | — |
| PCK1 deletion | Loss of Pck1 activity blocks chronological lifespan extension caused by water starvation. Knockout of PCK1 dramatically reduces chronological lifespan in both water (extreme DR) and glucose-containing medium. Deletion of SIR2 does not alter the lifespan of PCK1 deletion mutant, pck1-K514R, and pck1-K514Q mutants [19303850]. | Yeast | — | — | — |
| BNA6 deletion | Deletion of BNA6 (alias QPT1) has no effect on replicative lifespan and is not required for lifespan extension by DR, but is lethal with mutation of NPT1 [11000115]. Deletion of BNA6 decreases chronological lifespan [17110466]. | Yeast | — | — | — |
| PCK1 mutation | pck-1-K514Q mutation which abrogates enzymatic activity of Pck1, just like SIR2 deletion, extends chronological lifespan in water. Deletion of SIR2 does not alter the lifespan of PCK1 deletion mutant, pck1-K514R, and pck1-K514Q mutants [19303850]. | Yeast | — | — | — |
| ESA1 mutation | esa1-531 mutant has an even shorter chronological lifespan than PKA1 deletion mutant in both 2% glucose (ad libitum) and water (extreme DR) at 30 degree Celsius, a semipermissive temperature. At the permissive temperature (25 degree Celsius) there is little difference [19303850]. | Yeast | — | — | — |
| RAD1 mutation | Deletion of RAD1 has no effect on replicative lifespan [10207108]. | Yeast | — | — | — |
| GSH1 deletion | Deletion of GSH1 confers deficiency in glutathione biosynthesis and further increases chronological lifespan under 0.5% glucose restriction, but does not extend chronological lifespan under 2% glucose [18840459]. Therefore, GSH1 has a positive interaction with DR [18840459]. | Yeast | — | — | — |
| SCH9 Deletion | SCH9 deletion increases chronological lifespan by up to threefold. Stress-resistance transcription factors Msn2/Msn4 and protein kinase Rim15 are required for this life-extension. Deletion of the mitochondrial antioxidant enzyme superoxide dismutase gene SOD2 prevents the increased chronological lifespan caused by SCH9 deletion [11292860]. Mutations that decrease the activity of the Ras/Cyr1/PKA pathway also extend longevity and increase stress resistance by activating transcription factors Msn2/Msn4 and Sod2 [12855292]. SCH9 deletion mutants exhibit more than 3-fold extension of chronological lifespan. By day 9 of medium depletion all the wild-type cells were dead while 50% sch9 mutants survived [17710147]. Deletion of SCH9 also increases resistance to heat shock and oxidative stress [11292860], and increases replicative lifespan by 18% (in DBY746) [12586694]. SCH9 deletion increases the replicative lifespan by 40% in the alpha strain [18340043] and increases mean chronological lifespan by 97 - 246% (97, 133, 154, 226, 246) in diploid cells [21447998]. Mutation or deletion of SCH9 increases resistance to oxidants and extends chronological lifespan [11292860; 16286010]. The extended lifespan of SCH9 deletion mutants is not further extended by low glucose DR and is independent of Sir2 [16293764]. Deletion of RIM15 or GIS1 reverses chronological lifespan extension associated with sch9Delta. Water restriction further increases chronological lifespan of sch9Delta [18225956]. Deletion of SCH9 results in a longer chronological lifespan [21076178]. | Yeast | +18 to +300 | — | — |
| ERG3 deletion | Deletion of ERG3 decreases replicative lifespan under AL, cancels out replicative lifespan extension of 0.5% glucose DR and results under DR also into a shorter replicative lifespan than under AL [18690010]. | Yeast | — | — | — |
GenAge
GenDR
