DOS-3 mediates cell-non-autonomous DAF-16/FOXO activity in antagonizing age-related loss of C. elegans germline stem/progenitor cells

Zhifei Zhang, Haiyan Yang, Lei Fang, Guangrong Zhao, Jun Xiang (), Jialin C. Zheng () and Zhao Qin ()
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Zhifei Zhang: Tongji University
Haiyan Yang: Tongji University
Lei Fang: Tongji University
Guangrong Zhao: Tongji University
Jun Xiang: Tongji University School of Medicine
Jialin C. Zheng: Tongji Hospital Affiliated to Tongji University
Zhao Qin: Tongji University

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Age-related depletion of stem cells causes tissue degeneration and failure to tissue regeneration, driving aging at the organismal level. Previously we reported a cell-non-autonomous DAF-16/FOXO activity in antagonizing the age-related loss of germline stem/progenitor cells (GSPCs) in C. elegans, indicating that regulation of stem cell aging occurs at the organ system level. Here we discover the molecular effector that links the cell-non-autonomous DAF-16/FOXO activity to GSPC maintenance over time by performing a tissue-specific DAF-16/FOXO transcriptome analysis. Our data show that dos-3, which encodes a non-canonical Notch ligand, is a direct transcriptional target of DAF-16/FOXO and mediates the effect of the cell-non-autonomous DAF-16/FOXO activity on GSPC maintenance through activating Notch signaling in the germ line. Importantly, expression of a human homologous protein can functionally substitute for DOS-3 in this scenario. As Notch signaling controls the specification of many tissue stem cells, similar mechanisms may exist in other aging stem cell systems.

Date: 2024
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DOI: 10.1038/s41467-024-49318-6

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