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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kato, Michiko Lin, Su-ju Myers, Victoria Ilyas, Irtqa Tsang, Felicia Tsang, Matthew James, Christol |
| Description | Author Affiliation: Tsang F ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616.); James C ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616.); Kato M ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616.); Myers V ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616.); Ilyas I ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616.); Tsang M ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616.); Lin SJ ( From the Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis, California 95616 slin@ucdavis.edu.) |
| Abstract | Attenuated nutrient signaling extends the life span in yeast and higher eukaryotes; however, the mechanisms are not completely understood. Here we identify the Ssy1-Ptr3-Ssy5 (SPS) amino acid sensing pathway as a novel longevity factor. A null mutation of SSY5 (ssy5Δ) increases replicative life span (RLS) by â ¼50%. Our results demonstrate that several NAD(+) homeostasis factors play key roles in this life span extension. First, expression of the putative malate-pyruvate NADH shuttle increases in ssy5Δ cells, and deleting components of this shuttle, MAE1 and OAC1, largely abolishes RLS extension. Next, we show that Stp1, a transcription factor of the SPS pathway, directly binds to the promoter of MAE1 and OAC1 to regulate their expression. Additionally, deletion of SSY5 increases nicotinamide riboside (NR) levels and phosphate-responsive (PHO) signaling activity, suggesting that ssy5Δ increases NR salvaging. This increase contributes to NAD(+) homeostasis, partially ameliorating the NAD(+) deficiency and rescuing the short life span of the npt1Δ mutant. Moreover, we observed that vacuolar phosphatase, Pho8, is partially required for ssy5Δ-mediated NR increase and RLS extension. Together, our studies present evidence that supports SPS signaling is a novel NAD(+) homeostasis factor and ssy5Δ-mediated life span extension is likely due to concomitantly increased mitochondrial and vacuolar function. Our findings may contribute to understanding the molecular basis of NAD(+) metabolism, cellular life span, and diseases associated with NAD(+) deficiency and aging. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 20 |
| Volume Number | 290 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2015-05-15 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Carrier Proteins Metabolism Homeostasis Physiology Intracellular Signaling Peptides And Proteins Membrane Proteins NAD Saccharomyces Cerevisiae Proteins Saccharomyces Cerevisiae Serine Proteases Signal Transduction Alkaline Phosphatase Genetics Gene Deletion Gene Expression Regulation, Fungal Malate Dehydrogenase Vacuoles Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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