Abstract
Our recent study has revealed six plant extracts that slow yeast chronological aging more efficiently than any chemical compound yet described. The rate of aging in yeast is controlled by an evolutionarily conserved network of integrated signaling pathways and protein kinases. Here, we assessed how single-gene-deletion mutations eliminating each of these pathways and kinases affect the aging-delaying efficiencies of the six plant extracts. Our findings imply that these extracts slow aging in the following ways: 1) plant extract 4 decreases the efficiency with which the pro-aging TORC1 pathway inhibits the anti-aging SNF1 pathway; 2) plant extract 5 mitigates two different branches of the pro-aging PKA pathway; 3) plant extract 6 coordinates processes that are not assimilated into the network of presently known signaling pathways/protein kinases; 4) plant extract 8 diminishes the inhibitory action of PKA on SNF1; 5) plant extract 12 intensifies the anti-aging protein kinase Rim15; and 6) plant extract 21 inhibits a form of the pro-aging protein kinase Sch9 that is activated by the pro-aging PKH1/2 pathway.
Highlights
The budding yeast Saccharomyces cerevisiae is a beneficial model organism for the discovery of genes, signaling pathways and chemical compounds that slow cellular and organismal aging in eukaryotes across phyla [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15]
One of these aspects is the convergence of certain signaling pathways and protein kinases into a network that controls the rate of aging [1, 6, 11, 19,20,21,22,23,24,25,26,27,28,29,30,31]. This network integrates the following: 1) the pro-aging TORC1 pathway [32,33,34,35]; 2) the pro-aging PKA pathway [36,37,38,39,40]; 3) the pro-aging PKH1/2 (Pkb-activating kinase homolog) pathway [30, 41,42,43,44]; 4) the anti-aging SNF1 pathway [45,46,47,48,49,50]; 5) the anti-aging ATG pathway [5, 51,52,53,54,55,56,57,58]; 6) the pro-aging protein kinase Sch9, which is stimulated by the TORC1 and PKH1/2 pathways [11, 40, 42,43,44, 59, 60]; and 7) the anti-aging protein kinase Rim15, which is inhibited by the TORC1, PKA and PKH1/2 pathways [11, 37, 40, 59, 61, 62] (Figure 1)
We investigated the effects of the following single-gene-deletion mutations shown in Table 1: 1) tor1Δ, which impairs the pro-aging TORC1 pathway and increases CLS [32, 35]; 2) ras2Δ, which weakens the pro-aging PKA pathway and extends CLS [39]; 3) rim15Δ, which eliminates the anti-aging protein kinase Rim15 and shortens CLS [37]; 4) sch9Δ, which removes the pro-aging protein kinase Sch9 and increases CLS [37]; 5) pkh2Δ, which weakens the pro-aging PKH1/2 pathway and extends CLS [41, 42]; 6) snf1Δ, which impairs the anti-aging SNF1 pathway and decreases CLS [50, 62]; and 7) atg1Δ, which deteriorates the anti-aging ATG pathway and shortens CLS [51, 52]
Summary
The budding yeast Saccharomyces cerevisiae is a beneficial model organism for the discovery of genes, signaling pathways and chemical compounds that slow cellular and organismal aging in eukaryotes across phyla [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15]. Information flow along this network in yeast is controlled by such aging-delaying chemical compounds as resveratrol, rapamycin, caffeine, spermidine, myriocin, methionine sulfoxide, lithocholic acid and cryptotanshinone [3, 5, 6, 8,9,10, 12, 14, 43, 54, 74,75,76,77,78]
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