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Analysis of Cardiomyocyte Development using Immunofluorescence in Embryonic Mouse Heart
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Neddylation drives myofibrillogenesis in the developing heart.

Rodney Littlejohn1, Josue Zambrano-Carrasco1, Jianqiu Zou1

  • 1Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, Georgia, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 19, 2024
PubMed
Summary

Neddylation, a key process for cell function, is essential for heart development. Disrupting Nae1, a neddylation enzyme, in mice caused severe cardiac defects and embryonic lethality, highlighting neddylation's role in cardiogenesis.

Keywords:
NAE1Neddylationcardiac developmentmyofibril assembly

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Biochemistry

Background:

  • Neddylation is a crucial post-translational modification regulating protein function.
  • Its role in embryonic development and organogenesis is established, but its impact on heart development is unknown.

Purpose of the Study:

  • To investigate the role of neddylation in early cardiac development.
  • To determine the function of the NEDD8-activating enzyme 1 (Nae1) in cardiogenesis.

Main Methods:

  • Generated global and cardiac-specific Nae1 knockout mouse models using Nkx2-5Cre.
  • Performed histological analysis, transcriptomic profiling, and assessment of cardiomyocyte proliferation and mitochondrial function.

Main Results:

  • Global Nae1 deletion caused embryonic lethality before E8.5.
  • Cardiac-specific Nae1 knockout led to embryonic lethality around E12.5 with cardiac failure, characterized by thinning of the myocardium, reduced trabeculae, and impaired cardiomyocyte proliferation.
  • Loss of Nae1 disrupted sarcomere assembly, downregulated key cardiac transcription factors (NKX2-5, SRF), and impaired mitochondrial function.

Conclusions:

  • Neddylation, mediated by Nae1, is essential for embryonic heart development.
  • Neddylation is critical for cardiomyocyte proliferation, myofibrillogenesis, and maintaining cardiac function during development.