Metabolism Meets Translation: Dietary and Metabolic Influences on tRNA Modifications and Codon Biased Translation

Wiley Interdisciplinary Reviews - RNA, Journal Year: 2025, Volume and Issue: 16(2)

Published: March 1, 2025

ABSTRACT Transfer RNA (tRNA) is not merely a passive carrier of amino acids, but an active regulator mRNA translation controlling codon bias and optimality. The synthesis various tRNA modifications regulated by many “writer” enzymes, which utilize substrates from metabolic pathways or dietary sources. Metabolic bioenergetic pathways, such as one‐carbon (1C) metabolism the tricarboxylic acid (TCA) cycle produce essential for synthesis, S‐Adenosyl methionine (SAM), sulfur species, α‐ketoglutarate (α‐KG). activity these can directly impact decoding via regulating levels. In this review, we discuss complex interactions between diet, metabolism, modifications, translation. We how nutrient availability, bioenergetics, intermediates modulate modification landscape to fine‐tune protein synthesis. Moreover, highlight dysregulation metabolic‐tRNA contributes disease pathogenesis, including cancer, disorders, neurodegenerative diseases. also new emerging field GlycoRNA biology drawing parallels glycobiology diseases guide future directions in area. Throughout our discussion, links specific their metabolic/dietary precursors, diseases, emphasizing importance metabolism‐centric view understanding pathologies. Future research should focus on uncovering interplay cellular contexts. Addressing gaps will into novel interventions.

Language: Английский

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Gene expression profiles, potential targets and treatments of cardiac remodeling

Molecular and Cellular Biochemistry, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 5, 2024

Language: Английский

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Acetylation alchemy: how Nat10 shapes vascular health

European Heart Journal, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 28, 2024

Graphical AbstractNAT10 is a critical regulator in VSMC phenotypic transformation and vascular injury response.Open new tabDownload slide

Language: Английский

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Targeting the acetyltransferase NAT10 corrects pathologies in human frontotemporal neurons and extends lifespan in an in vivo Drosophila tauopathy model

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 22, 2024

ABSTRACT Disruption of the neuronal nuclear membrane and perturbation nucleocytoplasmic transport are features neurodegenerative diseases, including Alzheimer’s disease, that involve microtubule-associated protein tau (MAPT). We previously identified missense splicing mutations in MAPT gene, causal for frontotemporal dementia, result envelope deformation disrupted human neurons. This is most likely due to microtubule mechanical stress, similar observed Hutchinson-Gilford Progeria Syndrome (HGPS). A small molecule inhibitor acetyltransferase NAT10 has been shown correct defects HGPS by modulating dynamics. report here inhibition alters dynamics corrects lamina aberrant iPSC-derived FTD-MAPT Similarly, haploinsufficiency shape extend lifespan vivo a Drosophila model tauopathy. Our results show mediates pathologies tauopathies promising new therapeutic target these diseases.

Language: Английский

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Editorial overview: Epitranscriptomics: Exploring a new frontier in health and disease

Current Opinion in Genetics & Development, Journal Year: 2024, Volume and Issue: 89, P. 102271 - 102271

Published: Oct. 24, 2024

Language: Английский

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