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Nkx2-5 Second Heart Field Target Gene Ccdc117 Regulates DNA Metabolism and Proliferation

Anthony J Horton1, John Brooker1, William S Streitfeld1

  • 1Departments of Pediatrics and Obstetrics and Gynecology, Medical University of South Carolina, Charleston, SC, 29425, USA.

Scientific Reports
|February 12, 2019
PubMed

Insights

The cardiac transcription factor Nkx2-5 regulates Ccdc117, crucial for heart development. This discovery reveals Nkx2-5

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Molecular Genetics

Background:

  • Nkx2-5 is a vital cardiac transcription factor for outflow tract (OFT) and right ventricle (RV) development.
  • Nkx2-5 deficiency leads to hypoplasia and single ventricle phenotypes due to reduced Second Heart Field (SHF) progenitor cell proliferation.

Purpose of the Study:

  • To elucidate the precise role of Nkx2-5 in facilitating Second Heart Field (SHF) cell expansion during cardiac development.
  • To identify novel downstream targets of Nkx2-5 involved in SHF proliferation and cell cycle regulation.

Main Methods:

  • Investigated Nkx2-5's regulation of the novel target gene Ccdc117 in SHF cells.
  • Analyzed the interaction of Ccdc117 with the cytoplasmic iron-sulfur cluster assembly (CIA) complex.
  • Assessed the impact of Ccdc117 loss on cell proliferation, DNA synthesis, and DNA damage.

Main Results:

  • Nkx2-5 directly and positively regulates Ccdc117 expression in SHF progenitor cells.
  • Ccdc117 interacts with the CIA complex, essential for DNA repair and replication enzymes.
  • Loss of Ccdc117 impairs cell proliferation, delays G1-S transition, reduces DNA synthesis, and leads to DNA damage.

Conclusions:

  • Nkx2-5 plays a novel role in regulating cardiac cell cycle events during SHF expansion.
  • This regulation is mediated through Ccdc117's interaction with the CIA pathway, supporting DNA replication.
  • Findings highlight a new mechanism linking transcription factor activity to cell cycle control in heart development.

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