We have previously identified a
Hand1 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
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We have previously identified a
Hand1 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
Hand1 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
Hand1 enhancer mutants (
Hand1ΔST/ΔST) present with no observable phenotype. Assessment of lncRNA expression reveals that
Hand1ΔST/ΔST mutants effectively eliminate detectable lncRNA expression. Expression analysis within
Hand1ΔST/ΔST mutant hearts indicates higher levels of
Hand1 than in controls. The generation of
Hand1 compound heterozygous mutants with the
Hand1LacZ null allele (
Hand1ΔST/LacZ) also did not reveal any observable phenotypes. Together these data indicate that deletion of this
Hand1 enhancer and by consequence a family of murine-specific lncRNAs does not impact embryonic development in observable ways.
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