Spatiotemporal expression and transcriptional perturbations by long noncoding RNAs in the mouse brain
Name
Goff-2015-Spatiotemporal expre.pdf
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Author(s)
Goff, Loyal A.
Groff, Abigail F.
Sauvageau, Martin
Trayes-Gibson, Zachary
Sanchez-Gomez, Diana B.
Morse, Michael
Martin, Ryan D.
Elcavage, Lara E.
Liapis, Stephen C.
Gonzalez-Celeiro, Meryem
Date Issued
June 2015
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Goff, Loyal A., Abigail F. Groff, Martin Sauvageau, Zachary Trayes-Gibson, Diana B. Sanchez-Gomez, Michael Morse, Ryan D. Martin, et al. “Spatiotemporal Expression and Transcriptional Perturbations by Long Noncoding RNAs in the Mouse Brain.” Proc Natl Acad Sci USA 112, no. 22 (June 1, 2015): 6855–6862.
Version
Final published version
Abstract
Long noncoding RNAs (lncRNAs) have been implicated in numerous cellular processes including brain development. However, the in vivo expression dynamics and molecular pathways regulated by these loci are not well understood. Here, we leveraged a cohort of 13 lncRNA-null mutant mouse models to investigate the spatiotemporal expression of lncRNAs in the developing and adult brain and the transcriptome alterations resulting from the loss of these lncRNA loci. We show that several lncRNAs are differentially expressed both in time and space, with some presenting highly restricted expression in only selected brain regions. We further demonstrate altered regulation of genes for a large variety of cellular pathways and processes upon deletion of the lncRNA loci. Finally, we found that 4 of the 13 lncRNAs significantly affect the expression of several neighboring protein-coding genes in a cis-like manner. By providing insight into the endogenous expression patterns and the transcriptional perturbations caused by deletion of the lncRNA locus in the developing and postnatal mammalian brain, these data provide a resource to facilitate future examination of the specific functional relevance of these genes in neural development, brain function, and disease.
MIT Department
Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1073/pnas.1411263112
