FB2025_01 , released February 20, 2025
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Citation
Hayashi, Y., Kashio, S., Murotomi, K., Hino, S., Kang, W., Miyado, K., Nakao, M., Miura, M., Kobayashi, S., Namihira, M. (2022). Biosynthesis of S-adenosyl-methionine enhances aging-related defects in Drosophila oogenesis.  Sci. Rep. 12(1): 5593.
FlyBase ID
FBrf0253140
Publication Type
Research paper
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.
PubMed ID
PubMed Central ID
PMC8979982 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Sci. Rep.
    Title
    Scientific reports
    ISBN/ISSN
    2045-2322
    Data From Reference
    Alleles (3)
    Genes (2)
    Natural transposons (1)
    Insertions (2)
    Experimental Tools (1)
    Transgenic Constructs (3)