Whole mount in situ hybridization analysis of the 17 lncRNAs revealed that lncRNAs 2410006H16Rik and 4930500J02Rik were expressed in mouse hearts at E9.5. 4930500J02Rik, renamed Long Noncoding Cardiac-promoting RNA (LncCPR), was also enriched in postnatal and adult heart tissue. We hypothesized that the loss of LncCPR expression would directly affect cardiogenesis. To test this hypothesis, we performed functional studies of ESC differentiation after knocking out the LncCPR gene with the CRISPR/Cas9 system. We profiled the transcriptome of mouse ES cells after the loss of LncCPR expression. We found the downregulation of Mesp1 and cardiac transcription factors, as well as a significant reduction in contractility and levels of cardiac structural protein TNNT2. Our findings indicate that LncCPR is a novel, specific regulator of Mesp1, and therefore, of early cardiogenesis. SOURCE: Benjamin Soibam (soibamb@uhd.edu) -  university of houston-Downtown

Pluto Bioinformatics

GSE79499: LncRNA expression profiling of the early mesoderm reveals LncCPR as a novel regulator of cardiogenesis in mice