RNA secondary structure modulates FMRP’s bi-functional role in the microRNA pathway

Phillip Kenny, Stephanie Ceman

Research output: Contribution to journalReview article

Abstract

MicroRNAs act by post-transcriptionally regulating the gene expression of 30%–60% of mammalian genomes. MicroRNAs are key regulators in all cellular processes, though the mechanism by which the cell activates or represses microRNA-mediated translational regulation is poorly understood. In this review, we discuss the RNA binding protein Fragile X Mental Retardation Protein (FMRP) and its role in microRNA-mediated translational regulation. Historically, FMRP is known to function as a translational suppressor. However, emerging data suggests that FMRP has both an agonistic and antagonistic role in regulating microRNA-mediated translational suppression. This bi-functional role is dependent on FMRP’s interaction with the RNA helicase Moloney leukemia virus 10 (MOV10), which modifies the structural landscape of bound mRNA, therefore facilitating or inhibiting its association with the RNA-Induced Silencing Complex.

Original languageEnglish (US)
Article number985
JournalInternational Journal of Molecular Sciences
Volume17
Issue number6
DOIs
StatePublished - Jun 22 2016

Fingerprint

RNA
MicroRNAs
Fragile X Mental Retardation Protein
proteins
Proteins
Viruses
suppressors
Gene expression
RNA-Induced Silencing Complex
leukemias
genome
gene expression
regulators
RNA Helicases
Moloney murine leukemia virus
viruses
Genes
RNA-Binding Proteins
emerging
retarding

Keywords

  • FMRP
  • G-Quadruplex
  • MOV10
  • RNA binding proteins
  • Secondary structure
  • microRNA

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

RNA secondary structure modulates FMRP’s bi-functional role in the microRNA pathway. / Kenny, Phillip; Ceman, Stephanie.

In: International Journal of Molecular Sciences, Vol. 17, No. 6, 985, 22.06.2016.

Research output: Contribution to journalReview article

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