Literature DB >> 27986952

Deletion of the sclerotome-enriched lncRNA PEAT augments ribosomal protein expression.

David A Stafford1, Darwin S Dichmann1, Jessica K Chang2, Richard M Harland3.   

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.

Entities:  

Keywords:  BMP pathway; CRISPR/Cas9; long-noncoding RNA; ribosomal proteins; sclerotome

Mesh:

Substances:

Year:  2016        PMID: 27986952      PMCID: PMC5224379          DOI: 10.1073/pnas.1612069113

Source DB:  PubMed          Journal:  Proc Natl Acad Sci U S A        ISSN: 0027-8424            Impact factor:   11.205


  33 in total

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3.  A Universal Surrogate Reporter for Efficient Enrichment of CRISPR/Cas9-Mediated Homology-Directed Repair in Mammalian Cells.

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