Journal
EMBO JOURNAL
Volume 29, Issue 18, Pages 3082-3093Publisher
WILEY
DOI: 10.1038/emboj.2010.199
Keywords
non-coding RNA; nuclear domains; splicing factor; synaptogenesis; transcription
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Funding
- Institut pour la Recherche sur la Moelle epiniere et l'Encephale
- Association Francaise contre les Myopathies
- 7th framework program Moodinflame [222963]
- NIH/NIGMS [42694]
- NIH/NCI [5PO1CA013106-38]
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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.
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