1. Deletion of the sclerotome-enriched lncRNA PEAT augments ribosomal protein expression
- Author
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Stafford, David A, Dichmann, Darwin S, Chang, Jessica K, and Harland, Richard M
- Subjects
Genetics ,Animals ,Bone Morphogenetic Proteins ,CRISPR-Cas Systems ,Embryonic Development ,Gene Expression Regulation ,Developmental ,Mesoderm ,Mice ,Mice ,Inbred C57BL ,Mice ,Knockout ,Paired Box Transcription Factors ,RNA ,Long Noncoding ,RNA ,Ribosomal ,Ribosomal Proteins ,Sequence Deletion ,sclerotome ,CRISPR/Cas9 ,long-noncoding RNA ,ribosomal proteins ,BMP pathway - Abstract
To define a complete catalog of the genes that are activated during mouse sclerotome formation, we sequenced RNA from embryonic mouse tissue directed to form sclerotome in culture. In addition to well-known early markers of sclerotome, such as Pax1, Pax9, and the Bapx2/Nkx3-2 homolog Nkx3-1, the long-noncoding RNA PEAT (Pax1 enhancer antisense transcript) was induced in sclerotome-directed samples. Strikingly, PEAT is located just upstream of the Pax1 gene. Using CRISPR/Cas9, we generated a mouse line bearing a complete deletion of the PEAT-transcribed unit. RNA-seq on PEAT mutant embryos showed that loss of PEAT modestly increases bone morphogenetic protein target gene expression and also elevates the expression of a large subset of ribosomal protein mRNAs.
- Published
- 2017