Interventions

  • name effect species mean median maximum
    VPS27 deletion Under starvation conditions VPS27 deletion mutants have a dramatically reduced lifespan [20953148]. Yeast
    SAM1 deletion Deletion of SAM1 increases replicative lifespan by 20% in the alpha strain and 15% in the a strain [18340043]. Yeast +15 to +20
    OSH6 overexpression Elevation of OSH6 levels by an ERG6 promoter extends mean, median and maximum replicative lifespan by 39, 52 and 18% which is non-additive with 0.5% glucose restriction. It also extends the lifespan of NYV1 mutant [Geber et al., unpublished]. The long lifespan of Perg6-OSH6 is not further extended by deletion of TOR1 [22622083]. OSH6 overexpression decreases total cellular sterol content and reduces Lst8 protein levels. The CC domain of Osh6 is dispensable for longevity [Fusheng Tang, personal communication]. Yeast +39 +52 +18
    HES1 overexpression Elevation of HES1 levels by an ERG6 promoter reduces mean, median and maximum replicative lifespan by 25, 18 and 29% [Geber et al., unpublished] Yeast -25 -18 -29
    HES1 deletion Deletion of HES1 (alias OSH5) extends mean replicative lifespan by 27% and is non-addative with moderate DR. Deletion of OSH5 delays different steps of endocytosis, a sterol-requireing process. [Xia et al., unpublished]. Yeast
    INP53 deletion Deletion of INP53 increases mean replicative lifespan by 31% [16293764]. INP53 deletion increases replicative lifespan by 31% in the alpha strain and by 10% in the a strain [18340043]. Yeast +31
    ATG18 deletion The replicative lifespan of ATG18 deletion mutant is not shorter than that of wild-type under DR [18690010]. Yeast
    CKA2 deletion CKA2 deletion approximately doubles mean chronological lifespan under starvation/extreme DR in BY4741 also increases as well as as heat-shock resistance in SDC medium in the W303-1A and DBY746 genetic backgrounds [20657825]. Yeast
    CKB2 deletion Lack of Ckb2 promotes a modest but significant chronological lifespan extension and marked increase in yeat resistance [20657825]. Yeast
    VPS36 deletion VPS36 deletion mutant had a chronological lifespan as long as wild type BY4741. Thus, Vps36 is not necessary for the starvation/extreme DR-dependent lifespan extension [20657825]. Yeast
    CUP9 deletion Deletion of CUP9 increases replicative lifespan by 30% in the alpha and a strains [18340043]. Although CPU9 was identified as a potential long-lived mutant strain in a bar-code screen, the chronological lifespan of CUP9 deletion mutant is not significantly different from than of wild-type under starvation/extreme DR [20657825]. Yeast
    APD1 deletion Although APD1 was identified as a potential long-lived mutant strain in a bar-code screen, deletion of APD1 does not significantly affect chronological lifespan under starvation/extreme DR [20657825]. Yeast
    ZTA1 deletion Deletion of ZTA1 increases replicative lifespan by 15% in the alpha strain and decreased by 10% in the a strain [18340043]. Although ZTA1 was identified as a potential long-lived mutant strain in a bar-code screen, deletion of ZTA1 does not significantly affect chronological lifespan under starvation/extreme DR [20657825]. Yeast
    SSN2 deletion Although SSN2 was identified as a potential long-lived mutant strain in a bar-code screen, deletion of SSN2 does not significantly affect chronological lifespan under starvation/extreme DR [20657825]. Yeast
    ACB1 deletion ACB1 deletion extends chronological lifespan under starvation/extreme DR. Similar heat-shock resistance and resistance to a very hight concentration of acetic acid (but not resistance to oxidative stress) was enhanced by the deletion of ACB1. Deletion of ACB1 in W303-1A and DBY746 genetic backgrounds on synthetic complete media causes severe growth defects and sightly shorter lifespan and also heat-sensitivity [20657825]. Yeast
    TRM9 deletion TRM9 deletion almost triples mean chronological lifespan under starvation/extreme DR, increases heat resistance, but reduces resistance to acetic acid. Similar effect were present in the BY746 background in SDC medium [20657825]. Yeast
    RPL12B deletion Deletion of RPL12B increases mean replicative lifespan by 20% in the alpha strain [18423200] and by 22% in the remade strain, but increases non-significantly the mean replicative lifespan by 13% in the ORF collection [22377630]. RPL12B mutation promotes mean chronological longevity extension and heat-shock resistance but reduces acetic acid resistance under starvation/extreme DR. In DBY746 mutation of RPL12B almost doubles mean chronological lifespan in SDC medium and increases heat-shock resistance [20657825] Yeast
    ARO7 deletion Under starvation/extreme DR deletion of ARO7 increases mean chronological lifespan and confers higher resistance to heat-shock, but made cell more sensitive to acetic acid and leads to growth defects. In W303-1A background ARO7 deletion causes an even more severe growth defect and mutants are short-lived [20657825]. Yeast
    FAR3 deletion Deletion of FAR3 significantly reduces mean chronological lifespan under starvation/extreme DR relatively to wild-type [20657825]. Yeast
    FAR11 deletion Deletion of FAR11 significantly reduces mean chronological lifespan under starvation/extreme DR relatively to wild-type [20657825]. Yeast
    PPG1 deletion PPG1 deletion reduces significantly mean chronological lifespan under starvation/extreme DR [20657825]. Yeast
    BUL1 deletion Deletion of BUL1 does non-significantly reduces mean chronological lifespan under starvation/extreme DR [20657825]. Yeast
    PAN2 deletion Deletion mutant of PAN2 live approximately as long as wild-type under starvation/extreme DR [20657825]. Yeast
    OSH7 overexpression Overexpression of OSH7 extends mean replicative lifespan. PERG6-OSH7 does not extend the maximum lifespan significantly [Xia et al., unpublished]. Yeast
    BCY1 deletion Disruption in BCY1 by mutation results decreases mean and maximum replicative lifespan by 37 and 16% and is associated with increased PKA activity [8195187]. Yeast -37 -16
    Interventions are an extension of GenAge and GenDR.