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The one-carbon metabolism enzyme Ahcy is a redox sensor that modulates gene expression to protect against light stress-induced retinal degeneration

ABSTRACT: The one-carbon metabolism enzyme Ahcy is a redox sensor that modulates gene expression to protect against light stress-induced retinal degeneration

PROVIDER: PRJNA1249269 | ENA |

REPOSITORIES: ENA

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The one-carbon metabolism enzyme Ahcy is a redox sensor that modulates gene expression to protect against light stress-induced retinal degeneration

Project description:One-carbon metabolism influences the response to oxidative stress through antioxidant biosynthesis and the transcriptional status of the cell via epigenetic mechanisms. One-carbon metabolism is responsible for the production of the universal methyl donor, S-adenosylmethionine (SAM), which generates the potent methyltransferase inhibitor, S-adenosylhomocysteine (SAH). The essential metabolic enzyme, S-adenosylhomocysteinase (AHCY), functions within one-carbon metabolism and is the sole enzyme to catabolize the metabolite S-adenosylhomocysteine (SAH). Under oxidative stress conditions, AHCY becomes oxidized at a critical residue for its activity correlating with increased SAH abundance in the Drosophila head. Here, we profiled the photoreceptor transcriptome at a single time point after 3-hour blue light exposure relative to untreated controls in the Drosophila eye. We used RNAi expressed in all cells of the eye under longGMR-Gal4 to knockdown Ahcy and examined photoreceptor cells enriched using nuclei-immunoenrichment. As a control, we expressed non-specific RNAi against mCherry.

2025-09-04 | GSE294368 | GEO

The peroxiredoxin Asp f3 acts as redox sensor in Aspergillus fumigatus

Project description:The human pathogenic fungus Aspergillus fumigatus is readily eradicated by the innate immunity of immunocompetent human hosts, but can cause severe infections, such as invasive aspergillosis (IA), in immunocompromised individuals. During infection, the fungal redox homeostasis can be challenged by reactive oxygen (ROS) species, either derived from the oxidative burst of innate immune cells or the action of antifungal drugs. The peroxiredoxin Asp f3 was found to be essential to cause IA in mice, but how Asp f3 integrates to fungal redox homeostasis remains unknown. Here, we show that in vivo, Asp f3 acts as a sensor for ROS. While global transcription in fungal hyphae under minimal growth conditions was fully independent of Asp f3, a robust induction of the oxidative stress response required the presence of the peroxiredoxin. Hyphae devoid of Aspf 3 failed to activate several redox active genes, like members of the gliotoxin biosynthesis gene cluster and integral members of the Afyap1 regulon, the central activator of the ROS defence machinery in fungi. Upon deletion of the asp f3 gene Afyap1 displayed significantly reduced nuclear localization during ROS exposure, indicating that Asp f3 can act as an intracellular redox sensor for several target proteins

2021-06-03 | GSE173349 | GEO

Regulation of the circadian clock by the metabolic enzyme AHCY

Project description:Mammalian circadian rhythms are based on coupled transcriptional-translational feedback loops driven by the transcription factors CLOCK and BMAL1. Chromatin remodeling mechanisms are essential for the proper timing and extent of circadian gene expression. We report that the S-adenosylhomocysteine (SAH) hydrolysing enzyme AHCY binds to CLOCK-BMAL1 at chromatin and drives circadian transcription by promoting cyclic H3K4 trimethylation and recruitment of BMAL1 to chromatin.

2020-02-01 | GSE125720 | GEO

Regulation of the circadian clock by the metabolic enzyme AHCY

2021-01-11 | GSE126851 | GEO

The peroxiredoxin Asp f3 acts as redox sensor in Aspergillus fumigatus

Project description:The peroxiredoxin Asp f3 acts as redox sensor in Aspergillus fumigatus

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Next Generation Sequencing Facilitates Quantitative Analysis of WT AHCY E14.1 cell and T136A AHCY E14.1 cell

Project description:Purpose: To test the effect of AHCY O-GlcNAcylation on E14.1cell pluripotency and The goals of this study are to compare gene expression profiles of the WT AHCY rescue cells and the T136A AHCY rescue cells. Method:Total RNA was Trizol-extracted and purified from total RNA using poly-T oligo-attached magnetic beads. Fragmentation was carried out using divalent cations under elevated temperature in NEB. cDNA was synthesized using random hexamer primer and RNase H. The library fragments were purified with QiaQuick PCR kits and elution with EB buffer, then terminal repair A-tailing and adapter added were implemented. The clustering of the index-coded samples was performed on a cBot cluster generation system using HiSeq PE Cluster Kit v4-cBot-HS (Illumina) according to the manufacturer’s instructions. After cluster generation, the libraries were sequenced on an Illumina platform and 150 bp paired-end reads were generated. Results:Significant alterations in gene expression levels were observed, with 1351 genes upregulated and 979 genes downregulated in the T136A AHCY rescue cells

2020-03-01 | GSE143756 | GEO

Analysis of the senescence transcriptome after knockdown of AHCY

Project description:IMR90 ER:RAS cells were infected with 2 different lentiviral pGIPZ shRNAs against AHCY or with an empty vector (EV). We treated IMR90 ER:RAS cells with 4OHT to induce RAS activation or with vehicle (DMSO) as a non-senescent control. RNA was collected 6 days after the start of the experiment once the senescence program has been fully implemented. Our previous experiments showed that knockdown of AHCY prevents senescence. By performing RNAseq, we have unveiled that AHCY knockdown prevents upregulation of a set of genes essential for the onset of senescence and its associated secretory phenotype.

2022-07-19 | GSE155904 | GEO

Regulation of the circadian clock by the metabolic enzyme AHCY

Project description:Regulation of the circadian clock by the metabolic enzyme AHCY

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Project description:Regulation of the circadian clock by the metabolic enzyme AHCY

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Histone H3.1 is a chromatin embedded redox sensor triggered by tumor cells developing adaptive phenotypic plasticity and multi-drug resistance [ChIP-Seq]

Project description:Chromatin structure is regulated through histone post-translational modifications as well as histone variants. Although highly homologous, histone variants display unique amino acid sequences associated with specialized functions in gene transcription regulation. Abnormal incorporation of histone variants into chromatin contributes to cancer initiation, progression, metastasis, as well as, therapy resistance. The current study reports a novel epigenetic function of histone H3.1 as a redox sensor embedded in heterochromatin. We found that this new function depends on oxidation by nuclear ROS and lead to changes in the transcriptional profile of MCF10A cells.

2024-02-20 | GSE255615 | GEO

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