Increasing the number of ribosomal uL6 mRNA copies accelerates aging of the budding yeast.

BACKGROUND: Aging is a biological process from which there is no escape. Diverse factors contribute to aging, most notably cell energy metabolism. Ribosome biogenesis and translation are the two main energy-consuming processes that contribute to longevity. It has repeatedly been shown that translation disorders caused by deletion of ribosomal genes delay aging. However, the effect of increasing the amount of ribosomal proteins has remained elusive. METHODS AND RESULTS: We determine the relative level of the uL6A and uL6B mRNA derived from the genome and the plasmid. The appearance of additional copies of plasmid-derived uL6 leads to an increase in uL6A and uL6B derived from the BY4741 genome (mainly form B). The relative amount of mRNA of plasmid form B is several times greater than the amount of mRNA in plasmid form A. The level of mRNA derived from the plasmid is increased many times compared to the mRNA of genomic origin. Additionally, the study indicates that excess of uL6A is a limiting or even harmful factor in the reaction to stressful conditions. Therefore, our hypothesis states that uL6A transcription or mRNA uL6A degradation in yeast cells are tightly regulated. our data clearly demonstrate that aging is accelerated when additional copies of uL6 paralogs appear. CONCLUSION: Overexpression of both uL6A or uL6B accelerates aging in the budding yeast. The level of uL6A mRNA is tightly controlled by yeast cell. The uL6a protein plays a pivotal role in the response to environmental stress, including oxidative and osmotic stress, and thus may fall into the class of moonlighting ribosomal proteins with extra-ribosomal function.

Impact of curcumin on replicative and chronological aging in the Saccharomyces cerevisiae yeast.

Curcumin is a biologically active compound of vegetable origin which has a hormetic effect. Pro-health and anti-aging properties of curcumin have been known for years. The main benefit of curcumin is thought to be its anti-oxidative action. Despite vast amount of data confirming age-delaying activity of curcumin in various groups of organisms, so far little has been discovered about curcumin's impact on cell aging in the experimental model of the Saccharomyces cerevisiae budding yeast. We have been able to demonstrate that curcumin significantly increases oxidative stress and accelerates replicative and chronological aging of yeast cells devoid of anti-oxidative protection (with SOD1 and SOD2 gene deletion) and deprived of DNA repair mechanisms (RAD52). Interestingly, curcumin delays aging, probably through hormesis, of the wild-type strain BY4741.