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The homeodomain transcription factor NKX2-5 is known to be essential for both normal heart development and for heart function. But little is yet known about the identities of its downstream effectors or their function during differentiation of cardiac progenitor cells (CPCs). We have used transgenic analysis and CRISPR-mediated ablation to identify a cardiac enhancer of the  Furin  gene. The  Furin  gene, encoding a proprotein convertase, is directly repressed by NKX2-5. Deletion of  Furin  in CPCs is embryonic lethal, with mutant hearts showing a range of abnormalities in the outflow tract. Those defects are associated with a reduction in proliferation and premature differentiation of the CPCs. Deletion of  Furin  in differentiated cardiomyocytes results in viable adult mutant mice showing an elongation of the PR interval, a phenotype that is consistent with the phenotype of mice and human mutant for  Nkx2-5 . Our results show that  Furin  mediate some aspects of  Nkx2-5  function in the heart.

Furin, a transcriptional target of NKX2-5, has an essential role in heart development and function