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Inhibition of cardiomyocyte neddylation impairs embryonic cardiac morphogenesis

Rodney Littlejohn1, Josue Zambrano-Carrasco1, Jianqiu Zou1

  • 1Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA, United States.

Journal of Molecular and Cellular Cardiology
|October 22, 2024
PubMed

Insights

Neddylation, a key protein modification, is essential for heart development. Disrupting this process in mice impairs cardiomyocyte proliferation and Notch signaling, leading to severe heart defects and embryonic lethality.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Heart development involves complex spatiotemporal morphogenic events.
  • The role of posttranslational modifications, like neddylation, in cardiogenesis is not well understood.

Purpose of the Study:

  • To investigate the role of neddylation in coordinating heart development (cardiogenesis).
  • To understand how the protein neddylation pathway influences cardiomyocyte proliferation and signaling.

Main Methods:

  • Investigated neddylation by deleting Nae1 (a key neddylation enzyme) in the heart using Sm22αCre mice.
  • Analyzed heart development, cardiomyocyte proliferation, and Notch signaling in mutant embryos.

Main Results:

  • Complete abrogation of neddylation resulted in early embryonic lethality.
  • Mutant hearts showed impaired trabeculation and compact layer expansion.
  • Reduced cardiomyocyte proliferation was observed, linked to abnormal Notch signaling.

Conclusions:

  • Neddylation is crucial for normal heart development.
  • The neddylation pathway regulates cardiomyocyte proliferation and Notch signaling during cardiogenesis.

Keywords:
Heart developmentMyocardial hypoplasiaNEDD8NeddylationNotch signalingPosttranslational modification

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