miR-34 activity is modulated through 5'-end phosphorylation in response to DNA damage

Nat Commun. 2016 Mar 21:7:10954. doi: 10.1038/ncomms10954.

Abstract

MicroRNA (miRNA) expression is tightly regulated by several mechanisms, including transcription and cleavage of the miRNA precursor RNAs, to generate a mature miRNA, which is thought to be directly correlated with activity. MiR-34 is a tumour-suppressor miRNA important in cell survival, that is transcriptionally upregulated by p53 in response to DNA damage. Here, we show for the first time that there is a pool of mature miR-34 in cells that lacks a 5'-phosphate and is inactive. Following exposure to a DNA-damaging stimulus, the inactive pool of miR-34 is rapidly activated through 5'-end phosphorylation in an ATM- and Clp1-dependent manner, enabling loading into Ago2. Importantly, this mechanism of miR-34 activation occurs faster than, and independently of, de novo p53-mediated transcription and processing. Our study reveals a novel mechanism of rapid miRNA activation in response to environmental stimuli occurring at the mature miRNA level.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Argonaute Proteins / metabolism
  • Ataxia Telangiectasia Mutated Proteins / metabolism
  • Cell Line
  • DNA Damage / genetics*
  • Gene Expression Regulation
  • Humans
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Nuclear Proteins
  • Phosphorylation
  • Phosphotransferases
  • Transcription Factors
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • AGO2 protein, human
  • Argonaute Proteins
  • MIRN34 microRNA, human
  • MicroRNAs
  • Nuclear Proteins
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • CLP1 protein, human
  • Phosphotransferases
  • Ataxia Telangiectasia Mutated Proteins