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FMRP and MOV10 regulate Dicer1 expression and dendrite development.

Monica C Lannom1, Joshua Nielsen2, Aatiqa Nawaz1

  • 1Cell and Developmental Biology, University of Illinois, Urbana, Illinois, United States of America.

Plos One
|November 30, 2021
PubMed
Summary
This summary is machine-generated.

Fragile X syndrome is linked to reduced expression of Fragile X Mental Retardation Protein (FMRP). This study reveals FMRP and MOV10 regulate DICER1 expression, impacting miRNA production and neuronal development.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Fragile X syndrome (FXS) is caused by reduced Fragile X Mental Retardation Protein (FMRP) expression.
  • FMRP and MOV10 (RNA helicase Moloney Leukemia virus 10) are crucial cofactors in miRNA-mediated translation regulation.
  • Previous work established a functional association between MOV10 and FMRP.

Purpose of the Study:

  • To quantify the impact of reduced MOV10 and FMRP expression on dendritic morphology.
  • To investigate the hypothesis that MOV10 and FMRP regulate DICER1 expression.
  • To elucidate the molecular mechanism by which MOV10, FMRP, and AGO2 control miRNA production in neurons.

Main Methods:

  • Comparative analysis of dendritic morphology in murine neurons with reduced MOV10/FMRP versus Dicer1 knockout neurons.
  • Quantification of DICER1 expression in cells and tissues with altered MOV10 or FMRP levels.
  • Cross-linking immunoprecipitation (CLIP) assays to identify Dicer1 mRNA as a target of FMRP, MOV10, and AGO2.
  • Functional rescue experiments using a DICER1 transgene in Mov10 knockout neuroblastoma cells and heterozygote neurons.
  • Analysis of AGO2-associated microRNAs in Fmr1 knockout brain tissue.

Main Results:

  • Reduced MOV10 and FMRP expression in neurons phenocopied Dicer1 knockout neurons, showing impaired dendritic maturation.
  • DICER1 expression was significantly reduced in cells and tissues with decreased MOV10 or FMRP.
  • Dicer1 mRNA was confirmed as a CLIP target for FMRP, MOV10, and AGO2, with regulation occurring via the 3'UTR.
  • Introduction of a DICER1 transgene restored normal neurite outgrowth and branching in relevant cellular models.
  • A global reduction in AGO2-associated microRNAs was observed in Fmr1 knockout brains.

Conclusions:

  • The MOV10-FMRP-AGO2 complex plays a critical role in regulating DICER1 expression.
  • This regulation is essential for normal miRNA production and neuronal morphology.
  • This study uncovers a novel molecular mechanism contributing to the pathophysiology of Fragile X syndrome.