ArticleGenetics2009
Deleting the 14-3-3 protein Bmh1 extends life span in Saccharomyces cerevisiae by increasing stress response.
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Evidence of 14-3-3 proteins contributing to kinetochore integrity and chromosome congression during mitosis.Journal of cell science · 2024Article
- The yeast 14-3-3 proteins Bmh1 and Bmh2 regulate key signaling pathways.Frontiers in molecular biosciences · 2024Review
- Cyclin C-Cdk8 Kinase Phosphorylation of Rim15 Prevents the Aberrant Activation of Stress Response Genes.Frontiers in cell and developmental biology · 2022Article
- A Systematic Survey of Characteristic Features of Yeast Cell Death Triggered by External Factors.Journal of fungi (Basel, Switzerland) · 2021Review
- Regulation of trehalase activity by multi-site phosphorylation and 14-3-3 interaction.Scientific reports · 2021Article
- 14-3-3 Proteins Are on the Crossroads of Cancer, Aging, and Age-Related Neurodegenerative Disease.International journal of molecular sciences · 2019Review
- 14-3-3 Proteins: a window for a deeper understanding of fungal metabolism and development.World journal of microbiology & biotechnology · 2019Review
- Laboratory evolution of a glucose-phosphorylation-deficient, arabinose-fermenting S. cerevisiae strain reveals mutations in GAL2 that enable glucose-insensitive l-arabinose uptake.FEMS yeast research · 2018Article
- Less is more: Nutrient limitation induces cross-talk of nutrient sensing pathways with NADFrontiers in biology · 2015Article
- Reduced Ssy1-Ptr3-Ssy5 (SPS) signaling extends replicative life span by enhancing NAD+ homeostasis in Saccharomyces cerevisiae.The Journal of biological chemistry · 2015Article
- The 14-3-3 protein Bmh1 functions in the spindle position checkpoint by breaking Bfa1 asymmetry at yeast centrosomes.Molecular biology of the cell · 2014Article
- The yeast 14-3-3 proteins BMH1 and BMH2 differentially regulate rapamycin-mediated transcription.Bioscience reports · 2014Article
- Phenotypic and genotypic convergences are influenced by historical contingency and environment in yeast.Evolution; international journal of organic evolution · 2014Article
- Aging and cell death in the other yeasts, Schizosaccharomyces pombe and Candida albicans.FEMS yeast research · 2014Review
- The GCKIII kinase Sps1 and the 14-3-3 isoforms, Bmh1 and Bmh2, cooperate to ensure proper sporulation in Saccharomyces cerevisiae.PloS one · 2014Article
- Article
- In vivo phosphorylation of Ser21 and Ser83 during nutrient-induced activation of the yeast protein kinase A (PKA) target trehalase.The Journal of biological chemistry · 2012Article
- 14-3-3 protects against stress-induced apoptosis.Cell death & disease · 2012Article
- Untangling the Roles of Anti-Apoptosis in Regulating Programmed Cell Death using Humanized Yeast Cells.Frontiers in oncology · 2012Article
- Identification of potential calorie restriction-mimicking yeast mutants with increased mitochondrial respiratory chain and nitric oxide levels.Journal of aging research · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Enhanced stress response has been suggested to promote longevity in many species. Calorie restriction (CR) and conserved nutrient-sensing target of rapamycin (TOR) and protein kinase A (PKA) pathways have also been suggested to extend life span by increasing stress response, which protects cells from age-dependent accumulation of oxidative damages. Here we show that deleting the yeast 14-3-3 protein, Bmh1, extends chronological life span (CLS) by activating the stress response. 14-3-3 proteins are highly conserved chaperone-like proteins that play important roles in many cellular processes. bmh1Delta-induced heat resistance and CLS extension require the general stress-response transcription factors Msn2, Msn4, and Rim15. The bmh1Delta mutant also displays a decreased reactive oxygen species level and increased heat-shock-element-driven transcription activity. We also show that BMH1 genetically interacts with CR and conserved nutrient-sensing TOR- and PKA-signaling pathways to regulate life span. Interestingly, the level of phosphorylated Ser238 on Bmh1 increases during chronological aging, which is delayed by CR or by reduced TOR activities. In addition, we demonstrate that PKA can directly phosphorylate Ser238 on Bmh1. The status of Bmh1 phosphorylation is therefore likely to play important roles in life-span regulation. Together, our studies suggest that phosphorylated Bmh1 may cause inhibitory effects on downstream longevity factors, including stress-response proteins. Deleting Bmh1 may eliminate the inhibitory effects of Bmh1 on these longevity factors and therefore extends life span.
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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.