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A Reporter Assay to Analyze Intronic microRNA Maturation in Mammalian Cells
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A Reporter Assay to Analyze Intronic microRNA Maturation in Mammalian Cells

Published on: June 16, 2022

FUS stimulates microRNA biogenesis by facilitating co-transcriptional Drosha recruitment

Mariangela Morlando1, Stefano Dini Modigliani, Giulia Torrelli

  • 1Department of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Rome, Italy.

The EMBO Journal
|December 13, 2012
PubMed

Insights

The fused in sarcoma/translocated in liposarcoma (FUS/TLS) protein impacts microRNA production, particularly those vital for neuron function. FUS/TLS mutations may disrupt microRNA biogenesis in Amyotrophic Lateral Sclerosis (ALS).

Area of Science:

  • Molecular Biology
  • Neuroscience
  • Genetics

Background:

  • MicroRNA biogenesis is regulated by microprocessor components and co-factors.
  • Amyotrophic Lateral Sclerosis (ALS) is linked to mutations in proteins like FUS/TLS.

Purpose of the Study:

  • To investigate the role of FUS/TLS protein in microRNA biogenesis.
  • To explore the connection between FUS/TLS, microRNA dysregulation, and ALS pathogenesis.

Main Methods:

  • Chromatin recruitment assays to identify FUS/TLS binding sites.
  • Analysis of microRNA abundance following FUS/TLS depletion.
  • Assessment of Drosha levels at target gene loci.

Main Results:

  • FUS/TLS protein is recruited to chromatin at the transcription sites of specific microRNAs.
  • FUS/TLS binds to pri-microRNAs involved in neuronal function.
  • FUS/TLS depletion reduces microRNA biogenesis and Drosha levels at these loci.

Conclusions:

  • FUS/TLS is a key regulator of a subset of microRNAs essential for neuronal processes.
  • Altered FUS/TLS partitioning due to mutations may underlie microRNA biogenesis defects in ALS.
  • FUS/TLS contributes to neuronal microRNA homeostasis relevant to ALS.

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