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学術論文

Mutation of C. elegans demethylase spr-5 extends transgenerational longevity

MPS-Authors

Greer, E. L.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Becker, B.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Latza, C.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Antebi, A.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Shi, Y.
Max Planck Institute for Biology of Ageing, Max Planck Society;

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引用

Greer, E. L., Becker, B., Latza, C., Antebi, A., & Shi, Y. (2016). Mutation of C. elegans demethylase spr-5 extends transgenerational longevity. Cell Res, 26(2), 229-38. doi:10.1038/cr.2015.148.

要旨

Complex organismal properties such as longevity can be transmitted across generations by non-genetic factors. Here we demonstrate that deletion of the C. elegans histone H3 lysine 4 dimethyl (H3K4me2) demethylase, spr-5, causes a trans-generational increase in lifespan. We identify a chromatin-modifying network, which regulates this lifespan extension. We further show that this trans-generational lifespan extension is dependent on a hormonal signaling pathway involving the steroid dafachronic acid, an activator of the nuclear receptor DAF-12. These findings suggest that loss of the demethylase SPR-5 causes H3K4me2 mis-regulation and activation of a known lifespan-regulating signaling pathway, leading to trans-generational lifespan extension.