ArticlePLoS biology2019
The histone methyltransferase G9a regulates tolerance to oxidative stress-induced energy consumption.
Article in PLoS biology, 2019. 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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Who cites it
22 citing papers in PubMed, 52 citations in OpenAlex.
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- Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance.Nature reviews. Molecular cell biology · 2022Review
- Identification of an Epi-metabolic dependency on EHMT2/G9a in T-cell acute lymphoblastic leukemia.Cell death & disease · 2022Article
- Quinazoline Based HDAC Dual Inhibitors as Potential Anti-Cancer Agents.Molecules (Basel, Switzerland) · 2022Review
- The epigenetic regulator G9a attenuates stress-induced resistance and metabolic transcriptional programs across different stressors and species.BMC biology · 2021Article
- Glucose Protects Cochlear Hair Cells Against Oxidative Stress and Attenuates Noise-Induced Hearing Loss in Mice.Neuroscience bulletin · 2021Article
- Lipid Metabolism in Cancer Cells.Advances in experimental medicine and biology · 2021Article
- Unfolded Protein Response in Leukemia: From Basic Understanding to Therapeutic Opportunities.Trends in cancer · 2020Review
- The metabolome as a link in the genotype-phenotype map for peroxide resistance in the fruit fly, Drosophila melanogaster.BMC genomics · 2020Article
- Transposable elements contribute to the genomic response to insecticides inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- How Stress Facilitates Phenotypic Innovation Through Epigenetic Diversity.Frontiers in plant science · 2020Article
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress responses are crucial processes that require activation of genetic programs that protect from the stressor. Stress responses are also energy consuming and can thus be deleterious to the organism. The mechanisms coordinating energy consumption during stress response in multicellular organisms are not well understood. Here, we show that loss of the epigenetic regulator G9a in Drosophila causes a shift in the transcriptional and metabolic responses to oxidative stress (OS) that leads to decreased survival time upon feeding the xenobiotic paraquat. During OS exposure, G9a mutants show overactivation of stress response genes, rapid depletion of glycogen, and inability to access lipid energy stores. The OS survival deficiency of G9a mutants can be rescued by a high-sugar diet. Control flies also show improved OS survival when fed a high-sugar diet, suggesting that energy availability is generally a limiting factor for OS tolerance. Directly limiting access to glycogen stores by knocking down glycogen phosphorylase recapitulates the OS-induced survival defects of G9a mutants. We propose that G9a mutants are sensitive to stress because they experience a net reduction in available energy due to (1) rapid glycogen use, (2) an inability to access lipid energy stores, and (3) an overinduced transcriptional response to stress that further exacerbates energy demands. This suggests that G9a acts as a critical regulatory hub between the transcriptional and metabolic responses to OS. Our findings, together with recent studies that established a role for G9a in hypoxia resistance in cancer cell lines, suggest that G9a is of wide importance in controlling the cellular and organismal response to multiple types of stress.
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