Cell wall biosynthesis impairment affects the budding lifespan of the Saccharomyces cerevisiae yeast

The Saccharomyces cerevisiae yeast is one of the most widely used model in studies of cellular and organismal biology, including as aging and proliferation. Although several constraints of aging and budding lifespan have been identified, these processes have not yet been fully understood. Previous studies of aging in yeast have focused mostly on the molecular basics of the underlying mechanisms, while physical aspects, particularly those related to the cell wall, were rather neglected. In this paper, we examine for the first time, to our knowledge, the impact of cell wall biosynthesis disturbances on the lifespan in the budding yeast. We have used a set of cell wall mutants, including knr4\Delta, cts1\Delta, chs3\Delta, fks1\Delta and mnn9\Delta, which affect biosynthesis of all major cell wall compounds. Our results indicated that impairment of chitin biosynthesis and cell wall protein mannosylation reduced the budding lifespan, while disruption in the 1,3-\beta-glucan synthase activity had no adverse effect on that parameter. The impact varied in the severity and the most notable effect was observed for the mnn9\Delta mutant. What was interesting, in the case of the dysfunction of the Knr4 protein playing the role of the transcriptional regulator of cell wall chitin and glucan synthesis, the lifespan increased significantly. We also report the phenotypic characteristics of cell wall-associated mutants as revealed by imaging of the cell wall using transmission electron microscopy, scanning electron microscopy and atomic force microscopy. In addition, our findings support the conviction that achievement of the state of hypertrophy may not be the only factor that determines the budding lifespan

The links between hypertrophy, reproductive potential and longevity in the Saccharomyces cerevisiae yeast

The yeast Saccharomyces cerevisiae has long been used as a model organism for studying the basic mechanisms of aging. However, the main problem with the use of this unicellular fungus is the unit of "longevity". For all organisms, lifespan is expressed in units of time, while in the case of yeast it is defined by the number of daughter cells produced. Additionally, in yeast the phenotypic effects of mutations often show a clear dependence on the genetic background, suggesting the need for an analysis of strains representing different genetic backgrounds. Our results confirm the data presented in earlier papers that the reproductive potential is strongly associated with an increase in cell volume per generation. An excessive cell volume results in the loss of reproductive capacity. These data clearly support the hypertrophy hypothesis. The time of life of all analysed mutants, with the exception of sch9D, is the same as in the case of the wild-type strain. Interestingly, the 121% increase of the fob1D mutant's reproductive potential compared to the sfp1D mutant does not result in prolongation of the mutant's time of life (total lifespan)

Dependence of the yeast Saccharomyces cerevisiae post-reproductive lifespan on the reproductive potential

The lifespan of budding yeast cells is divided into two stages: reproductive and post-reproductive. The post-reproductive stage of the yeast's lifespan has never been characterized before. We have analyzed the influence of various mutations on the post-reproductive (PRLS) and replicative (RLS) lifespans. The results indicate that PRLS demonstrates an inverse relationship with RLS. The observed lack of differences in the total lifespan (TLS) (expressed in units of time) of strains differing up to five times in RLS (expressed in the number of daughters formed) suggests the necessity of revision of opinions concerning the use of yeast as a model organism of gerontology

Enzymatic Defense Response of Apple Aphid Aphis pomi to Increased Temperature

Climate change, and in particular the increase in temperature we are currently observing, can affect herbivorous insects. Aphids, as poikilothermic organisms, are directly exposed to temperature increases that influence their metabolism. Heat stress causes disturbances between the generations and the neutralization of reactive oxygen species (ROS). The aim of this work is focused on explaining how the aphid, using the example of Aphis pomi, responds to abiotic stress caused by temperature increase. The experiment was carried out under controlled conditions at three temperatures: 20, 25, and 28 °C. In the first stage, changes in the activity of enzymatic markers (superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), β-glucosidase, polyphenol oxidase (PPO), and peroxidase (POD)) were determined in aphid tissues, at each temperature. In the second stage, microcalorimetry monitored changes in heat emitted by aphids, at each temperature. Our results showed that A. pomi defense responses varied depending on temperature and were highest at 28 °C. The flexible activity of enzymes and increase in the metabolic rate played the role of adaptive mechanisms and ran more effectively at higher temperatures. The A. pomi thus protected itself against ROS excessive induction and the aphids were able to respond quickly to environmental stress

Daughters of the budding yeast from old mothers have shorter replicative lifespans but not total lifespans. Are DNA damage and rDNA instability the factors that determine longevity?

<p>Although a lot of effort has been put into the search for factors responsible for aging in yeast mother cells, our knowledge of cellular changes in daughter cells originating from old mothers is still very limited. It has been shown that an old mother is not able to compensate for all negative changes within its cell and therefore transfers them to the bud. In this paper, we show for the first time that daughter cells of an old mother have a reset lifespan expressed in units of time despite drastic reduction of their budding lifespan, which suggests that a single yeast cell has a fixed programmed longevity regardless of the time point at which it was originated. Moreover, in our study we found that longevity parameters are not correlated with the rDNA level, DNA damage, chromosome structure or aging parameters (budding lifespan and total lifespan).</p