ArticleScientific reports2022
Biosynthesis of S-adenosyl-methionine enhances aging-related defects in Drosophila oogenesis.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 18 citations in OpenAlex.
- Prenols and prenoic acids in metabolism, disease, and aging.Journal of lipid research · 2026Review
- Somatic gene repression ensures physical segregation of germline and soma in Drosophila embryos.EMBO reports · 2026Article
- A fastFly · 2025Article
- Metabolic regulation in the senescence process of stem cells.Stem cells translational medicine · 2025Review
- Disruption of oocyte SUMOylation impacts critical regulatory processes during folliculogenesis in mice†.Biology of reproduction · 2025Article
- Genomic Assessment of the Contribution of theInternational journal of molecular sciences · 2023Article
- The effect of growth hormone on the metabolome of follicular fluid in patients with diminished ovarian reserve.Reproductive biology and endocrinology : RB&E · 2023Observational
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10 authors at 5 institutions in 1 country.
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Abstract
Tissue aging is a major cause of aging-related disabilities and a shortened life span. Understanding how tissue aging progresses and identifying the factors underlying tissue aging are crucial; however, the mechanism of tissue aging is not fully understood. Here we show that the biosynthesis of S-adenosyl-methionine (SAM), the major cellular donor of methyl group for methylation modifications, potently accelerates the aging-related defects during Drosophila oogenesis. An aging-related increase in the SAM-synthetase (Sam-S) levels in the germline leads to an increase in ovarian SAM levels. Sam-S-dependent biosynthesis of SAM controls aging-related defects in oogenesis through two mechanisms, decreasing the ability to maintain germline stem cells and accelerating the improper formation of egg chambers. Aging-related increases in SAM commonly occur in mouse reproductive tissue and the brain. Therefore, our results raise the possibility suggesting that SAM is the factor related to tissue aging beyond the species and tissues.
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