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<p>Transcription factors such as <i>Tbx5</i>, <i>Gata4</i>, <i>Mef2c</i> and <i>Pitx2</i> are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the <i>miR-200</i> family. Inhibition of a single <i>miR-200</i> family member within the cluster results in defects of the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire <i>miR-200</i> family results in a ventricular septal defect and embryonic lethality by embryonic day (E)16.5. Inhibition of each <i>miR-200</i> family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing reveals an immature cardiomyocyte cell state, suggesting reduced differentiation of these cells. The <i>miR-200</i> family members are critical regulators of early cardiac development through maintaining cardiomyocyte differentiation and maturation. In this report, we identify several transcription factors regulated by <i>miR-200</i> during heart development, a role for <i>miR-200</i> in specific heart defects, and an abnormal cardiomyocyte population.</p>

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Single-nuclei multiomics analysis identifies abnormal cardiomyocytes in a murine model of cardiac development

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月29日

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  • Riley Leonard,
  • Yi Zhao,
  • Steven Eliason,
  • Kathy Zimmerman,
  • Ariana Batz,
  • Cathy J. Hatcher,
  • Robert M. Weiss,
  • Mason Sweat,
  • Xiao Li,
  • Brad A. Amendt

摘要

Transcription factors such as Tbx5, Gata4, Mef2c and Pitx2 are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the miR-200 family. Inhibition of a single miR-200 family member within the cluster results in defects of the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire miR-200 family results in a ventricular septal defect and embryonic lethality by embryonic day (E)16.5. Inhibition of each miR-200 family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing reveals an immature cardiomyocyte cell state, suggesting reduced differentiation of these cells. The miR-200 family members are critical regulators of early cardiac development through maintaining cardiomyocyte differentiation and maturation. In this report, we identify several transcription factors regulated by miR-200 during heart development, a role for miR-200 in specific heart defects, and an abnormal cardiomyocyte population.