Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway

Peng Jin, Daniela C Zarnescu, Spephanie Ceman, Mika Nakamoto, Julie Mowrey, Thomas A. Jongens, David L. Nelson, Kevin Moses, Stephen T. Warren

Research output: Contribution to journalArticle

470 Citations (Scopus)

Abstract

Fragile X syndrome is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is a selective RNA-binding protein which forms a messenger ribonucleoprotein (mRNP) complex that associates with polyribosomes. Recently, mRNA ligands associated with FMRP have been identified. However, the mechanism by which FMRP regulates the translation of its mRNA ligands remains unclear. MicroRNAs are small noncoding RNAs involved in translational control. Here we show that in vivo mammalian FMRP interacts with microRNAs and the components of the microRNA pathways including Dicer and the mammalian ortholog of Argonaute 1 (AGO1). Using two different Drosophila melanogaster models, we show that AGO1 is critical for FMRP function in neural development and synaptogenesis. Our results suggest that FMRP may regulate neuronal translation via microRNAs and links microRNAs with human disease.

Original languageEnglish (US)
Pages (from-to)113-117
Number of pages5
JournalNature Neuroscience
Volume7
Issue number2
DOIs
StatePublished - Feb 2004
Externally publishedYes

Fingerprint

Fragile X Mental Retardation Protein
MicroRNAs
Molecular Biology
Ligands
Fragile X Syndrome
Small Untranslated RNA
Messenger RNA
RNA-Binding Proteins
Polyribosomes
Protein Biosynthesis
Drosophila melanogaster

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway. / Jin, Peng; Zarnescu, Daniela C; Ceman, Spephanie; Nakamoto, Mika; Mowrey, Julie; Jongens, Thomas A.; Nelson, David L.; Moses, Kevin; Warren, Stephen T.

In: Nature Neuroscience, Vol. 7, No. 2, 02.2004, p. 113-117.

Research output: Contribution to journalArticle

Jin, P, Zarnescu, DC, Ceman, S, Nakamoto, M, Mowrey, J, Jongens, TA, Nelson, DL, Moses, K & Warren, ST 2004, 'Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway', Nature Neuroscience, vol. 7, no. 2, pp. 113-117. https://doi.org/10.1038/nn1174
Jin, Peng ; Zarnescu, Daniela C ; Ceman, Spephanie ; Nakamoto, Mika ; Mowrey, Julie ; Jongens, Thomas A. ; Nelson, David L. ; Moses, Kevin ; Warren, Stephen T. / Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway. In: Nature Neuroscience. 2004 ; Vol. 7, No. 2. pp. 113-117.
@article{431b8ed024b5451f8c5d1164d0bbe3e0,
title = "Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway",
abstract = "Fragile X syndrome is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is a selective RNA-binding protein which forms a messenger ribonucleoprotein (mRNP) complex that associates with polyribosomes. Recently, mRNA ligands associated with FMRP have been identified. However, the mechanism by which FMRP regulates the translation of its mRNA ligands remains unclear. MicroRNAs are small noncoding RNAs involved in translational control. Here we show that in vivo mammalian FMRP interacts with microRNAs and the components of the microRNA pathways including Dicer and the mammalian ortholog of Argonaute 1 (AGO1). Using two different Drosophila melanogaster models, we show that AGO1 is critical for FMRP function in neural development and synaptogenesis. Our results suggest that FMRP may regulate neuronal translation via microRNAs and links microRNAs with human disease.",
author = "Peng Jin and Zarnescu, {Daniela C} and Spephanie Ceman and Mika Nakamoto and Julie Mowrey and Jongens, {Thomas A.} and Nelson, {David L.} and Kevin Moses and Warren, {Stephen T.}",
year = "2004",
month = "2",
doi = "10.1038/nn1174",
language = "English (US)",
volume = "7",
pages = "113--117",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "2",

}

TY - JOUR

T1 - Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway

AU - Jin, Peng

AU - Zarnescu, Daniela C

AU - Ceman, Spephanie

AU - Nakamoto, Mika

AU - Mowrey, Julie

AU - Jongens, Thomas A.

AU - Nelson, David L.

AU - Moses, Kevin

AU - Warren, Stephen T.

PY - 2004/2

Y1 - 2004/2

N2 - Fragile X syndrome is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is a selective RNA-binding protein which forms a messenger ribonucleoprotein (mRNP) complex that associates with polyribosomes. Recently, mRNA ligands associated with FMRP have been identified. However, the mechanism by which FMRP regulates the translation of its mRNA ligands remains unclear. MicroRNAs are small noncoding RNAs involved in translational control. Here we show that in vivo mammalian FMRP interacts with microRNAs and the components of the microRNA pathways including Dicer and the mammalian ortholog of Argonaute 1 (AGO1). Using two different Drosophila melanogaster models, we show that AGO1 is critical for FMRP function in neural development and synaptogenesis. Our results suggest that FMRP may regulate neuronal translation via microRNAs and links microRNAs with human disease.

AB - Fragile X syndrome is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is a selective RNA-binding protein which forms a messenger ribonucleoprotein (mRNP) complex that associates with polyribosomes. Recently, mRNA ligands associated with FMRP have been identified. However, the mechanism by which FMRP regulates the translation of its mRNA ligands remains unclear. MicroRNAs are small noncoding RNAs involved in translational control. Here we show that in vivo mammalian FMRP interacts with microRNAs and the components of the microRNA pathways including Dicer and the mammalian ortholog of Argonaute 1 (AGO1). Using two different Drosophila melanogaster models, we show that AGO1 is critical for FMRP function in neural development and synaptogenesis. Our results suggest that FMRP may regulate neuronal translation via microRNAs and links microRNAs with human disease.

UR - http://www.scopus.com/inward/record.url?scp=1642540373&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1642540373&partnerID=8YFLogxK

U2 - 10.1038/nn1174

DO - 10.1038/nn1174

M3 - Article

C2 - 14703574

AN - SCOPUS:1642540373

VL - 7

SP - 113

EP - 117

JO - Nature Neuroscience

JF - Nature Neuroscience

SN - 1097-6256

IS - 2

ER -