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The three mutants, sch9Δ, ras2Δ, tor1Δ share the same phenotype: longer chronological life span.
The three yeast mutants sch9Δ, ras2Δ, tor1Δ show extended chronological life span up to three folds.
The age defined by the absolute time after birth (budding) is called the chronological life span (CLS) [8].
Our results in yeast suggest that reduction of mitochondrial activities closely relates to extension of the yeast chronological life span.
Fig. 3 shows the influence of the different α-syns on the chronological life span of various yeast strains.
Shorten chronological life span in autophagy-defective mutants may be at least partly attributed to mitochondria dysfunction.
Mutation in Sir2, a gene necessary for asymmetric segregation in yeast [8], resulted in a longer chronological life span under caloric restriction [18].
In a large scale screening in yeast, several genes that encode components of the nutrient-responsive TOR pathway were found to increase the chronological life span [8].
Matecic et al. reported that raising medium pH to 6.0 also induces the extension of chronological life span in atg mutants [28].
Deletion of ras2 or down-regulation of cyr1 in the Ras2/cAMP/PKA pathway nearly doubles the chronological life span of yeast [6], [7].
Calorie restriction (CR), which resembles the starvation conditions used to assess chronological life span, causes longevity extension in all the ageing model systems.
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