Abstract
Despite many controversies, the yeast Saccharomyces cerevisiae continues to be used as a model organism for the study of aging. Numerous theories and hypotheses have been created for several decades, yet basic mechanisms of aging have remained unclear. Therefore, the principal aim of this work is to propose a possible mechanism leading to increased longevity in yeast. In this paper, we suggest for the first time that there is a link between decreased metabolic activity, fertility and longevity expressed as time of life in yeast. Determination of reproductive potential and total lifespan with the use of fob1Δ and sfp1Δ mutants allows us to compare the “longevity” presented as the number of produced daughters with the longevity expressed as the time of life. The results of analyses presented in this paper suggest the need for a change in the definition of longevity of yeast by taking into consideration the time parameter. The mutants that have been described as “long-lived” in the literature, such as the fob1Δ mutant, have an increased reproductive potential but live no longer than their standard counterparts. On the other hand, the sfp1Δ mutant and the wild-type strain produce a similar number of daughter cells, but the former lives much longer. Our results demonstrate a correlation between the decreased efficiency of the translational apparatus and the longevity of the sfp1Δ mutant. We suggest that a possible factor regulating the lifespan is the rate of cell metabolism. To measure the basic metabolism of the yeast cells, we used the isothermal microcalorimetry method. In the case of sfp1Δ, the flow of energy, ATP concentration, polysome profile and translational fitness are significantly lower in comparison with the wild-type strain and the fob1Δ mutant.Electronic supplementary materialThe online version of this article (doi:10.1007/s11357-015-9868-8) contains supplementary material, which is available to authorized users.
Highlights
The yeast Saccharomyces cerevisiae is one of the model organisms used in research connected with aging processes
Post-reproductive lifespan (PRLS) of the fob1Δ mutant is strongly shortened, whereas that of the sfp1Δ mutant is substantially extended when compared to the wild-type strain (Fig. 1c)
The total lifespan TLS of the fob1Δ mutant, treated as a Blongevity mutant^, does not differ from the total lifespan of the standard strain, in contrast to the sfp1Δ mutant which has a significantly increased TLS (Fig. 1d). These results confirm the previous findings that deletion of the FOB1 gene does not result in longevity expressed in units of time, but only if lifespan is expressed as the number of daughters produced
Summary
The yeast Saccharomyces cerevisiae is one of the model organisms used in research connected with aging processes. In 1959, Mortimer and Johnston observed that a single mother cell of the budding yeast S. cerevisiae has a limited reproductive ability (Mortimer and Johnston 1959). It was supposed to be a model for research on aging of the cells capable of division in higher eukaryotes, including humans (Polymenis and Kennedy 2012). A group of scientists led by Muller suggested that a limited reproductive potential of a cell may be connected with budding processes rather than aging (Muller et al 1980). At the end of 1980s, it was postulated that accumulation of a Bsenescence factor^ in mother yeast cells during subsequent cycles is the reason for limitation of the number of reproduction cycles. A direct consequence of the choice of budding as a means of asexual reproduction of yeast cells is the asymmetric distribution of damaged macromolecules between the products of cytokinesis
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