Multiple knockout mouse models reveal lincRNAs are required for life and brain development

eLife - Tập 2
Martin Sauvageau1,2, Loyal A. Goff1,3,2, Simona Lodato1,2, Boyan Bonev1,2, Abigail F. Groff1,2, Chiara Gerhardinger1,2, Diana B. Sanchez-Gomez4, Ezgi Hacisuleyman1,2, Eric V. Li4, Matthew Spence4, Stephen C. Liapis1,2, William Mallard1,2, Michael Morse1,2, Mavis R. Swerdel5, Michael F D’Ecclessis5, Jennifer C. Moore6, Venus Lai7, Guochun Gong7, George D. Yancopoulos7, David Frendewey7, Manolis Kellis1,3, Ronald P. Hart5, David M. Valenzuela7, Paola Arlotta1,2, John L. Rinn1,8,2
1Broad Institute of MIT and Harvard, Cambridge, United States
2Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, United States
3Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, United States
4Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, United States.
5Department of Cell Biology and Neuroscience, Rutgers, The State University of New Jersey, New Brunswick, United States
6Department of Genetics, Rutgers, The State University of New Jersey, New Brunswick, United States
7Regeneron Pharmaceuticals Inc., Tarrytown, United States
8Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, United States

Tóm tắt

Many studies are uncovering functional roles for long noncoding RNAs (lncRNAs), yet few have been tested for in vivo relevance through genetic ablation in animal models. To investigate the functional relevance of lncRNAs in various physiological conditions, we have developed a collection of 18 lncRNA knockout strains in which the locus is maintained transcriptionally active. Initial characterization revealed peri- and postnatal lethal phenotypes in three mutant strains (Fendrr, Peril, and Mdgt), the latter two exhibiting incomplete penetrance and growth defects in survivors. We also report growth defects for two additional mutant strains (linc–Brn1b and linc–Pint). Further analysis revealed defects in lung, gastrointestinal tract, and heart in Fendrr−/− neonates, whereas linc–Brn1b−/− mutants displayed distinct abnormalities in the generation of upper layer II–IV neurons in the neocortex. This study demonstrates that lncRNAs play critical roles in vivo and provides a framework and impetus for future larger-scale functional investigation into the roles of lncRNA molecules.

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