ArticleAging2015
Distinct regulation of Maf1 for lifespan extension by Protein kinase A and Sch9.
Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Mitochondrial Metabolism in the Spotlight: Maintaining Balanced RNAP III Activity Ensures Cellular Homeostasis.International journal of molecular sciences · 2023Article
- Maf1 limits RNA polymerase III-directed transcription to preserve genomic integrity and extend lifespan.Cell cycle (Georgetown, Tex.) · 2021Article
- RNA Polymerase III, Ageing and Longevity.Frontiers in genetics · 2021Review
- Review
- The GATA Transcription Factor Gaf1 Represses tRNAs, Inhibits Growth, and Extends Chronological Lifespan Downstream of Fission Yeast TORC1.Cell reports · 2020Article
- Maf1-dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan.Aging cell · 2020Article
- Conserved roles of glucose in suppressing reactive oxygen species-induced cell death and animal survival.Aging · 2019Article
- Maf1 ameliorates cardiac hypertrophy by inhibiting RNA polymerase III through ERK1/2.Theranostics · 2019Article
- Longer life through an odd Pol enzyme.Nature · 2017Article
- Article
- The C-Box Region of MAF1 Regulates Transcriptional Activity and Protein Stability.Journal of molecular biology · 2017Article
- Stress resistance and lifespan are increased in C. elegans but decreased in S. cerevisiae by mafr-1/maf1 deletion.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Protein kinase A (PKA) and Sch9 regulates cell growth as well as lifespan in Saccharomyces cerevisiae. Maf1 is a RNA polymerase III (PolIII) inhibitor that tailors 5S rRNA and tRNA production in response to various environmental cues. Both PKA and Sch9 have been shown to phosphorylate Maf1 in vitro at similar amino acids, suggesting a redundancy in Maf1 regulation. However, here we find that activating PKA by bcy1 deletion cannot replace Sch9 for Maf1 phosphorylation and cytoplasmic retention; instead, such modulation lowers Maf1 protein levels. Consistently, loss of MAF1 or constitutive PKA activity reverses the stress resistance and the extended lifespan of sch9Δ cells. Overexpression of MAF1 partially rescues the extended lifespan of sch9Δ in bcy1Δsch9Δ mutant, suggesting that PKA suppresses sch9Δ longevity at least partly through Maf1 abundance. Constitutive PKA activity also reverses the reduced tRNA synthesis and slow growth of sch9Δ, which, however, is not attributed to Maf1 protein abundance. Therefore, regulation of lifespan and growth can be decoupled. Together, we reveal that lifespan regulation by PKA and Sch9 are mediated by Maf1 through distinct mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.