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A post-transcriptional mechanism pacing expression of neural genes with precursor cell differentiation status

Author

Listed:
  • Weijun Dai

    (School of Biological Sciences, Nanyang Technological University)

  • Wencheng Li

    (Biochemistry, and Molecular Genetics, Rutgers New Jersey Medical School)

  • Mainul Hoque

    (Biochemistry, and Molecular Genetics, Rutgers New Jersey Medical School)

  • Zhuyun Li

    (School of Biological Sciences, Nanyang Technological University)

  • Bin Tian

    (Biochemistry, and Molecular Genetics, Rutgers New Jersey Medical School)

  • Eugene V. Makeyev

    (School of Biological Sciences, Nanyang Technological University
    MRC Centre for Developmental Neurobiology, King’s College London)

Abstract

Nervous system (NS) development relies on coherent upregulation of extensive sets of genes in a precise spatiotemporal manner. How such transcriptome-wide effects are orchestrated at the molecular level remains an open question. Here we show that 3′-untranslated regions (3′ UTRs) of multiple neural transcripts contain AU-rich cis-elements (AREs) recognized by tristetraprolin (TTP/Zfp36), an RNA-binding protein previously implicated in regulation of mRNA stability. We further demonstrate that the efficiency of ARE-dependent mRNA degradation declines in the neural lineage because of a decrease in the TTP protein expression mediated by the NS-enriched microRNA miR-9. Importantly, TTP downregulation in this context is essential for proper neuronal differentiation. On the other hand, inactivation of TTP in non-neuronal cells leads to dramatic upregulation of multiple NS-specific genes. We conclude that the newly identified miR-9/TTP circuitry limits unscheduled accumulation of neuronal mRNAs in non-neuronal cells and ensures coordinated upregulation of these transcripts in neurons.

Suggested Citation

  • Weijun Dai & Wencheng Li & Mainul Hoque & Zhuyun Li & Bin Tian & Eugene V. Makeyev, 2015. "A post-transcriptional mechanism pacing expression of neural genes with precursor cell differentiation status," Nature Communications, Nature, vol. 6(1), pages 1-11, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8576
    DOI: 10.1038/ncomms8576
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