Quasi-programmed aging of budding yeast: a trade-off between programmed processes of cell proliferation, differentiation, stress response, survival and death defines yeast lifespan

Abstract

Recent findings suggest that evolutionarily distant organisms share the key features of the aging process and exhibit similar mechanisms of its modulation by certain genetic, dietary and pharmacological interventions. The scope of this review is to analyze mechanisms that in the yeast Saccharomyces cerevisiae underlie: (1) the replicative and chronological modes of aging; (2) the convergence of these 2 modes of aging into a single aging process; (3) a programmed differentiation of aging cell communities in liquid media and on solid surfaces; and (4) longevity-defining responses of cells to some chemical compounds released to an ecosystem by other organisms populating it. Based on such analysis, we conclude that all these mechanisms are programs for upholding the long-term survival of the entire yeast population inhabiting an ecological niche; however, none of these mechanisms is a ʺprogram of agingʺ - i.e., a program for progressing through consecutive steps of the aging process.

Caloric restriction controls stationary phase survival through Protein Kinase A (PKA) and cytosolic pH

“…PKA activity may have evolved to balance between fast growth and survival, with dysregulations affecting both (Zakrzewska et al, ; Zaman et al, ). Such a growth‐versus‐survival trade‐off is similar to the model of quasi‐programmed aging, according to which the age‐related death would be an aftermath of the growth programme (Arlia‐Ciommo, Piano, Leonov, Svistkova, & Titorenko, ). Alternatively, the death of a fraction of the population may be beneficial too, as it releases nutrients that can be used for growth by the remaining (genetically identical) more adapted cell subpopulation (Fabrizio et al, ).…”

Six plant extracts delay yeast chronological aging through different signaling pathways

“…In the future, it would be important to validate the above hypothesis by investigating how each of the six aging-delaying PEs impacts the physical links that connect individual hubs and nodes of the chronological aging network shown in Figure 9. These links are known to be mainly activating or inhibiting phosphorylations and dephosphorylations of certain target proteins that are transiently or permanently reside in various cellular locations, including the plasma membrane, vacuole, nucleus, mitochondria or cytosol [1, 2, 5, 6, 10–12, 14, 21–76, 84–86]. …”

Aspirin Causes Lipid Accumulation and Damage to Cell Membrane by Regulating DCI1/OLE1 in Saccharomyces cerevisiae

“…The budding yeast S. cerevisiae is a beneficial model organism for many biological systems. 9 It not only has a relatively short life span and is stable in both haploid and diploid forms, 10,11 but also can quickly and efficiently respond to stress phenomena resulting from environmental or nutritional insult. 12 Due to these advanced properties, S. cerevisiae has been widely applied to biochemical, genetic, and cytological studies in fundamental cellular processes.…”