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Emerging roles for sphingolipids in cellular aging

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Abstract

Aging is a gradual loss of physiological functions as organisms’ progress in age. Although aging in multicellular organisms is complex, some fundamental mechanisms and pathways may be shared from the single cellular yeast to human. Budding yeast Saccharomyces cerevisiae has been established model system for aging studies. A yeast cell divides asymmetrically to produce two cells that differ in size and age. The one that is smaller coming from bud is a newborn cell that with a full replicative potential head irrespective of the replicative age of its mother—the larger cell from which the bud grows out before division. The age asymmetry between daughter and mother is thought to be dependent on asymmetric segregation of certain factors such as protein aggregates, extrachromosomal DNA (ERCs) and dysfunctional organelles during successive cell divisions of the yeast replicative lifespan (RLS). It is also thought that certain plasma membrane proteins, in particular multidrug-resistant (MDR) proteins, asymmetrically partition between the mother and the bud based on the age of the polypeptides. Functional decline associated with the molecular aging of those proteins contributes to the fitness decline at advance age. In our recent study, we showed that sphingolipids facilitate the age-dependent segregation of MDRs between daughter and mother cell. In this review, we highlight and discuss the potential mechanisms by which sphingolipids regulate the aging process in yeast and cells of vertebrate animals including human.

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Acknowledgements

This work was supported by the Grant R35 GM118172 from the National Institutes of Health to R. Li. The authors apologize to the researchers whose work could not be cited or not cited fully due to space limitation.

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Correspondence to Pushpendra Singh.

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Authors declare that they have no conflict of interest.

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Communicated by M. Kupiec.

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Singh, P., Li, R. Emerging roles for sphingolipids in cellular aging. Curr Genet 64, 761–767 (2018). https://doi.org/10.1007/s00294-017-0799-z

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  • DOI: https://doi.org/10.1007/s00294-017-0799-z

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