Despite many controversies, the yeast continues to be used as a

Despite many controversies, the yeast continues to be used as a model organism for the study of aging. number of child 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 mutant. We suggest that a possible factor regulating the lifespan is usually the rate of cell metabolism. To measure the basic metabolism of the yeast cells, we used the isothermal microcalorimetry method. In the case of mutant. Electronic supplementary material The online version of this article (doi:10.1007/s11357-015-9868-8) contains supplementary material, which is available to authorized users. is usually 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 has a limited reproductive ability (Mortimer and Johnston 1959). Gerontological studies have been centered by a model of aging called replicative aging, which in its initial version informs us about the number of child cells produced by an individual cell. 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 senescence factor in mother yeast cells during subsequent cycles is usually the reason for limitation of the number of reproduction cycles. That factor is usually supposed not to be transferred to the bud, or it can only be exceeded down to the bud in a small amount. That is usually why the daughters HMR (virgin cells) maintain full reproductive potential irrespective of the reproductive age of the mother cell. One of the first candidates proposed as the senescence factor was extrachromosomal rDNA circles (Sinclair and Guarente 1997). The role of that factor was also assigned to the damaged mitochondria (Delaney et al. 2013; Lai et al. 2002), oxidatively damaged proteins (Aguilaniu et al. 2003) or thermal aggregates (Erjavec et al. 2007). A direct Gefitinib result of the choice of budding as a means of asexual reproduction of yeast cells is usually the asymmetric distribution of damaged macromolecules between the products of cytokinesis. Reproductive potential can be regulated by knockout or overexpression of genes. A number of genes have been recognized which, by being knocked out, can increase or decrease reproductive potential of cells (at the.g. or yeast is usually totally different. Because of that, each factor or mutation that causes an increase in the reproductive potential is usually considered to have a life-prolonging role. There are details which indicate that conveying yeast lifespan as a number of decades without taking Gefitinib into account the time parameter can alter dramatically the meaning of the obtained results (Zadrag-Tecza et al. 2013). It was shown that the time of life of the analyzed mutants and their standard counterparts is usually relatively constant (differing by less than 30?%), irrespective of their genetic background. On the other hand, the value of replicative lifespan (number of daughters) can differ up to five Gefitinib occasions. This clearly shows that the applied models are completely not proportional, and hence drawing findings concerning longevity of yeast on such basis seems far-fetched (Zadrag-Tecza et al. 2013; Zadrag et al. 2008). The idea that longevity of animals depends on the rate of.