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MicroRNA mir-34 provides robustness to environmental stress response via the DAF-16 network in C. elegans

Isik, Meltem, Blackwell, T. Keith, Berezikov, Eugene·2016·Scientific Reports
DOI 10.1038/srep36766PMC PMC5131338
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Abstract

Diverse stresses and aging alter expression levels of microRNAs, suggesting a role for these posttranscriptional regulators of gene expression in stress modulation and longevity. Earlier studies demonstrated a central role for the miR-34 family in promoting cell cycle arrest and cell death following stress in human cells. However, the biological significance of this response was unclear. Here we show that in C. elegans mir-34 upregulation is necessary for developmental arrest, correct morphogenesis, and adaptation to a lower metabolic state to protect animals against stress-related damage. Either deletion or overexpression of mir-34 lead to an impaired stress response, which can largely be explained by perturbations in DAF-16/FOXO target gene expression. We demonstrate that mir-34 expression is regulated by the insulin signaling pathway via a negative feedback loop between miR-34 and DAF-16/FOXO. We propose that mir-34 provides robustness to stress response programs by controlling noise in the DAF-16/FOXO-regulated gene network.

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Metadata

Authors
Isik, M., Blackwell, T. K., & Berezikov, E.
Venue
Scientific Reports
Publisher
Springer Science and Business Media LLC
Published
2016-12-01
Volume
6
Issue
1
ISSN
2045-2322
DOI
10.1038/srep36766
PMC
PMC5131338
Cited by
50
References
5
Language
en
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