| Summary: | We have previously identified a <i>Hand1</i> transcriptional enhancer that drives expression within the septum transversum, the origin of the cells that contribute to the epicardium. This enhancer directly overlaps a common exon of a predicted family of long non-coding RNAs (lncRNA) that are specific to mice. To interrogate the necessity of this <i>Hand1</i> enhancer, as well as the importance of these novel lncRNAs, we deleted the enhancer sequences, including the common exon shared by these lncRNAs, using genome editing. Resultant homozygous <i>Hand1</i> enhancer mutants (<i>Hand1<b><sup>Δ</sup></b><sup>ST/<b>Δ</b>ST</sup></i>) present with no observable phenotype. Assessment of lncRNA expression reveals that <i>Hand1<b><sup>Δ</sup></b><sup>ST/<b>Δ</b>ST</sup></i> mutants effectively eliminate detectable lncRNA expression. Expression analysis within <i>Hand1<b><sup>Δ</sup></b><sup>ST/<b>Δ</b>ST</sup></i> mutant hearts indicates higher levels of <i>Hand1</i> than in controls. The generation of <i>Hand1</i> compound heterozygous mutants with the <i>Hand1<sup>LacZ</sup></i> null allele (<i>Hand1<b><sup>Δ</sup></b><sup>ST/LacZ</sup></i>) also did not reveal any observable phenotypes. Together these data indicate that deletion of this <i>Hand1</i> enhancer and by consequence a family of murine-specific lncRNAs does not impact embryonic development in observable ways.
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