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Neuroreport. 1998 Feb 16;9(3):477-81.

No evidence for disruption of normal patterns of mRNA localization in dendrites or dendritic transport of recently synthesized mRNA in FMR1 knockout mice, a model for human fragile-X mental retardation syndrome.

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1
Department of Neuroscience and Neurosurgery, University of Virginia Health Sciences Center, Charlottesville 22908, USA.

Abstract

Recent studies have revealed that FMRP, the gene product of the fragile-X gene FMR1, is an RNA-binding protein. These and other data have led to the idea that FMRP may play a role in targeting mRNAs for transport to synaptic sites. The present study evaluated whether a null mutation of FMR1 disrupts the patterns of localization of three mRNAs that are present constitutively in dendrites (the mRNAs for MAP2, CAMII kinase and dendrin), or disrupt the rapid dendritic transport of the mRNA for activity-regulated cytoskeletal protein (ARC), coded for by an immediate-early gene. In situ hybridization analyses revealed that the patterns of mRNA localization in dendrites and the dendritic transport of ARC mRNA are indistinguishable from normal in FMR1 knockout mice. These results indicate that FMRP does not play an obligatory role in targeting this set of mRNAs to dendrites, although it might be involved in targeting other dendritic mRNAs yet to be identified.

[Indexed for MEDLINE]

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