A long nuclear-retained non-coding RNA regulates synaptogenesis by modulating gene expression

Bernard, D., Prasanth, K. V. , Tripathi, V., Colasse, S., Nakamura, T., Xuan, Z., Zhang, M. Q. , Sedel, F., Jourdren, L., Coulpier, F., Triller, A., Spector, D. L., Bessis, A. (2010) A long nuclear-retained non-coding RNA regulates synaptogenesis by modulating gene expression. EMBO Journal, 29 (18). pp. 3082-3093.

URL: http://www.ncbi.nlm.nih.gov/pubmed/20729808
DOI: 10.1038/emboj.2010.199

Abstract

A growing number of long nuclear-retained non-coding RNAs (ncRNAs) have recently been described. However, few functions have been elucidated for these ncRNAs. Here, we have characterized the function of one such ncRNA, identified as metastasis-associated lung adenocarcinoma transcript 1 (Malat1). Malat1 RNA is expressed in numerous tissues and is highly abundant in neurons. It is enriched in nuclear speckles only when RNA polymerase II-dependent transcription is active. Knock-down studies revealed that Malat1 modulates the recruitment of SR family pre-mRNA-splicing factors to the transcription site of a transgene array. DNA microarray analysis in Malat1-depleted neuroblastoma cells indicates that Malat1 controls the expression of genes involved not only in nuclear processes, but also in synapse function. In cultured hippocampal neurons, knock-down of Malat1 decreases synaptic density, whereas its over-expression results in a cell-autonomous increase in synaptic density. Our results suggest that Malat1 regulates synapse formation by modulating the expression of genes involved in synapse formation and/or maintenance.

Item Type: Paper
Subjects: bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > ncRNA
CSHL Authors:
Communities: CSHL labs > Spector lab
CSHL labs > Zhang lab
Depositing User: Brian Soldo
Date: 2010
Date Deposited: 04 Apr 2012 19:11
Last Modified: 28 Jan 2015 15:59
PMCID: PMC2944070
Related URLs:
URI: https://repository.cshl.edu/id/eprint/25644

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