Abstract:
:Transposons are known to participate in tissue aging, but their effects on aged stem cells remain unclear. Here, we report that in the Drosophila ovarian germline stem cell (GSC) niche, aging-related reductions in expression of Piwi (a transposon silencer) derepress retrotransposons and cause GSC loss. Suppression of Piwi expression in the young niche mimics the aged niche, causing retrotransposon depression and coincident activation of Toll-mediated signaling, which promotes Glycogen synthase kinase 3 activity to degrade β-catenin. Disruption of β-catenin-E-cadherin-mediated GSC anchorage then results in GSC loss. Knocking down gypsy (a highly active retrotransposon) or toll, or inhibiting reverse transcription in the piwi-deficient niche, suppresses GSK3 activity and β-catenin degradation, restoring GSC-niche attachment. This retrotransposon-mediated impairment of aged stem cell maintenance may have relevance in many tissues, and could represent a viable therapeutic target for aging-related tissue degeneration.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Lin KY,Wang WD,Lin CH,Rastegari E,Su YH,Chang YT,Liao YF,Chang YC,Pi H,Yu BY,Chen SH,Lin CY,Lu MY,Su TY,Tzou FY,Chan CC,Hsu HJdoi
10.1038/s41467-020-16858-6subject
Has Abstractpub_date
2020-06-19 00:00:00pages
3147issue
1issn
2041-1723pii
10.1038/s41467-020-16858-6journal_volume
11pub_type
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