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Expression analysis of Saccharomyces cerevisiae wild-type and rph1Δ two and 24 hours following menadione treatment

ABSTRACT: Investigation of whole genome gene expression changes at short (2 hours) and extended (24 hours) timepoints in wild-type Saccharomyces cerevisiae treated with 50 μM menadione during exponential growth compared to an rph1Δ strain Transient treatment with 50 μM menadione elevates mitochondrial ROS and extends chronological lifespan in yeast. Deletion of RPH1, a H3K36me3 histone demethylase, block chronological lifespan extension. This study aimed to identify Rph1p-dependent gene expression changes induced by menadione treatment that may support chronological lifespan extension. Reference: Bonawitz, N.D., Chatenay-Lapointe, M., Wearn, C.M., and Shadel, G.S. (2008). Expression of the rDNA-encoded mitochondrial protein Tar1p is stringently controlled and responds differentially to mitochondrial respiratory demand and dysfunction. Curr Genet 54, 83-94. A 24 chip study using total RNA recovered from two separate cultures each of Saccharomyces cerevisiae wild-type DBY2006 and rph1Δ. Each chip measures expression levels of 5,777 transcripts from NCBI build June 2008 with 8 probes per transcript and 3 replicate probe sets.

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Elizabeth Schroeder

PROVIDER: E-GEOD-45383 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression analysis of Saccharomyces cerevisiae wild-type and rph1Δ two and 24 hours following menadione treatment

Project description:Investigation of whole genome gene expression changes at short (2 hours) and extended (24 hours) timepoints in wild-type Saccharomyces cerevisiae treated with 50 μM menadione during exponential growth compared to an rph1Δ strain Transient treatment with 50 μM menadione elevates mitochondrial ROS and extends chronological lifespan in yeast. Deletion of RPH1, a H3K36me3 histone demethylase, block chronological lifespan extension. This study aimed to identify Rph1p-dependent gene expression changes induced by menadione treatment that may support chronological lifespan extension. Reference: Bonawitz, N.D., Chatenay-Lapointe, M., Wearn, C.M., and Shadel, G.S. (2008). Expression of the rDNA-encoded mitochondrial protein Tar1p is stringently controlled and responds differentially to mitochondrial respiratory demand and dysfunction. Curr Genet 54, 83-94.

2013-03-22 | GSE45383 | GEO

Expression data from ferulic acid treated C. elegans

Project description:Gene expression in N2 worms treated with 500 μM or 0 μM ferulic acid, at days 5. Effects of ferulic acid in C. elegans gene expression is studied, as our results indicate a lifespan extension effect produced by this molecule. RNA-seq were used to detail the global programme of gene expression underlying the lifespan extension and identified distinct classes of up/down-regulated genes in animals treated with ferulic acid.

2021-05-05 | GSE171836 | GEO

Structural clusters of histone H3 and H4 residues regulate chronological lifespan in Saccharomyces cerevisiae [Other]

Project description:We have performed a comprehensive analysis of the involvement of histone H3 and H4 residues in the regulation of chronological lifespan in yeast. Residues where substitution resulted in the most pronounced lifespan extension are all on the exposed face of the nucleosome, with the exception of H3E50, which is present on the lateral surface, between two DNA gyres. Other residues that had a more modest effect on lifespan extension were concentrated at the extremities of the H3-H4 dimer, suggesting a role in stabilizing the dimer in its nucleosome frame. Residues implicated in a reduced lifespan were buried in the histone handshake motif, suggesting that these mutations destabilize the octamer structure. All residues exposed on the disk and that caused lifespan extension are known to interact with Sir3. We find that substitution of H4K16 and H4H18 cause Sir3 to redistribute from telomeres and silent mating loci to secondary positions, often enriched for Rap1 or Abf1 binding sites, whereas H3E50 does not. The redistributed Sir3 cause transcriptional repression at most of the new loci, including of genes where null mutants were previously shown to extend chronological lifespan. The transcriptomic profiles of H4K16 and H4H18 mutant strains are very similar, and compatible with a DNA replication stress response. This is distinct from the transcriptomic profile of H3E50, which matches strong induction of oxidative phosphorylation. We propose that different clusters of H3 and H4 residues are involved in either binding to non-histone proteins, or in destabilizing the association of the nucleosome DNA, or disrupting binding of a H3-H4 dimer in the nucleosome, or disturbing the structural stability of the octamer, each category impacting on chronological lifespan through a different path.

2019-11-09 | GSE140160 | GEO

Structural clusters of histone H3 and H4 residues regulate chronological lifespan in Saccharomyces cerevisiae [ChIP-seq]

2019-12-03 | GSE141306 | GEO

Structural clusters of histone H3 and H4 residues regulate chronological lifespan in Saccharomyces cerevisiae [RNA-seq]

2019-12-13 | GSE141973 | GEO

Structural clusters of histone H3 and H4 residues regulate chronological lifespan in Saccharomyces cerevisiae [Sir3 ChIP-seq]

2019-12-03 | GSE141317 | GEO

The nucleosome remodeling and deacetylase (NuRD) complex mediates the mitochondrial unfolded protein response and longevity in C. elegans

Project description:Mitochondrial stress during development causes widespread changes in chromatin structure to promote mitochondrial unfolded protein response (UPRmt), perpetuating an early response across a lifetime results in lifespan extension. We found that the nucleosome remodeling and deacetylase (NuRD) complex interact with the transcription factor DVE-1 to initiate the global chromatin condensation and induce the UPRmt in animals experienced with mild mitochondrial dysfunction. The condensed chromatin structure can be well maintained into later life that is beneficial for lifespan extension. Moreover, overexpression of the core component of the NuRD complex is sufficient to induce the UPRmt response and longevity in C. elegans. Thus, a transient mitochondrial stress response during early development is established and propagated into later life through the NuRD-dependent chromatin remodeling pathway to extend lifespan.

2020-07-31 | GSE143904 | GEO

TORC1 signaling pathway inhibition by rapamycin and caffeine affect lifespan, global gene expression and cell proliferation of fission yeast

Project description:Target of rapamycin complex 1 (TORC1) is implicated in growth control and aging from yeast to humans. Fission yeast is emerging as a popular model organism to study TOR signaling, although rapamycin has been thought to not affect cell growth in this organism. Here we analyzed the effects of rapamycin and caffeine, singly and combined, on multiple cellular processes in fission yeast. The two drugs led to diverse and specific phenotypes that depended on TORC1 signaling pathway inhibition, including prolonged chronological lifespan, inhibition of global translation, inhibition of cell growth and division, and reprogramming of global gene expression mimicking nitrogen starvation. Rapamycin and caffeine differentially affected these various TORC1-dependent processes. Combined drug treatment augmented most phenotypes and effectively blocked cell growth. Although rapamycin showed a much more subtle effect on global translation than did caffeine, rapamycin was more effective in prolonging chronological lifespan. Rapamycin prolonged the lifespan of non-growing cells only when applied during the growth phase but not when applied after cells had stopped proliferation. The doses of rapamycin and caffeine strongly correlated with growth inhibition and with lifespan extension. This comprehensive analysis will inform future studies into TORC1 function and cellular aging in fission yeast and beyond.

2013-05-05 | E-MTAB-1489 | biostudies-arrayexpress

Sit4 genetically interacts with Vps27 to regulate mitochondrial function and lifespan in Saccharomyces cerevisiae

Project description:Sit4 is a PP2A-like Ser/Thr protein phosphatase implicated in the regulation of cellular processes important for cell survival during aging. We have previously shown that SIT4 deletion promotes vacuolar acidification, mitochondrial derepression and oxidative stress resistance, increasing yeast chronological lifespan. In this study, we performed a proteomic analysis of isolated vacuoles and yeast genetic interaction analysis to unravel how Sit4 influences vacuolar and mitochondrial function. By employing high-resolution mass spectrometry, we show that sit4Δ vacuolar membranes were enriched in Vps27 and Hse1, two proteins that are part of the endosomal sorting complex required for transport-0 complex. In addition, SIT4 exhibited a negative genetic interaction with VSP27, as sit4∆vps27∆ double mutants had a shortened lifespan compared to sit4∆ and vps27∆ single mutants. Our results also show that Vps27 did not increase sit4∆ lifespan by improving protein trafficking or vacuolar sorting pathways. However, Vps27 was critical for iron homeostasis and mitochondrial function in sit4∆ cells, as sit4∆vps27∆ double mutants exhibited high iron levels, impaired mitochondrial respiration and mitochondrial DNA (mtDNA) depletion. These findings show for the first-time a cross-talk between Sit4 and Vps27, providing new insights into the mechanisms governing chronological lifespan.

2024-05-24 | PXD048450 | Pride

PGAM5 promotes lasting FoxO activation after developmental mitochondrial stress and extends lifespan in Drosophila

Project description:The mitochondrial unfolded protein response (UPRmt) has been associated with long lifespan across metazoans. In Caenorhabditis elegans, mild developmental mitochondrial stress activates UPRmt reporters and extends lifespan. We show that similar developmental stress is necessary and sufficient to extend Drosophila lifespan, and identify Phosphoglycerate Mutase 5 (PGAM5) as a mediator of this response. Developmental mitochondrial stress leads to activation of FoxO, via Apoptosis Signal-regulating Kinase 1 (ASK1) and Jun-N-terminal Kinase (JNK). This activation persists into adulthood and induces a select set of chaperones, many of which have been implicated in lifespan extension in flies. Persistent FoxO activation can be reversed by a high- protein diet in adulthood, through mTORC1 and GCN-2 activity. Accordingly, the observed lifespan extension is prevented on a high-protein diet and in FoxO-null flies. The diet-sensitivity of this pathway has important implications for interventions that seek to engage the UPRmt to improve metabolic health and longevity.

2017-10-25 | GSE106105 | GEO

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