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Understanding the role of Shroom3 in the developing mouse myocardium
Jennifer L Carleton1,2, Rami R Halabi1,2, Jessica A Willson1,3
1Children's Health Research Institute, Victoria Research Labs, London, Ontario, Canada.
Plos One
|September 8, 2025
Summary
SHROOM3 protein is crucial for heart development, but its loss in heart muscle cells does not cause congenital heart defects. Other cell types, like cardiac neural crest cells, are likely responsible for SHROOM3-related heart abnormalities.
Area of Science:
- Developmental Biology
- Cardiovascular Biology
- Cell Biology
Background:
- Actin cytoskeleton regulation is vital for development.
- SHROOM3, an actin-binding protein, is essential for neural tube closure.
- SHROOM3 is expressed in the developing heart, and its dysfunction is linked to congenital heart defects.
Purpose of the Study:
- To investigate the role of SHROOM3 in cardiac development.
- To determine if SHROOM3 acts cell-autonomously in cardiomyocytes.
- To identify the cell types responsible for SHROOM3-associated heart defects.
Main Methods:
- Gene trap mouse models for full-body SHROOM3 loss.
- Conditional knockout mouse models (floxed SHROOM3 with Nkx2-5-Cre) for myocardial-specific SHROOM3 loss.
- Phenotypic analysis of embryos and adult mice, including heart morphology and cardiomyocyte size.
Main Results:
- Homozygous SHROOM3 loss in embryos caused exencephaly and congenital heart defects (ventricular septal defects, semilunar valve abnormalities, ventricular wall thinning).
- Adult heterozygous SHROOM3 loss led to ventricular thinning and reduced cardiomyocyte size.
- Myocardial-specific SHROOM3 loss did not result in significant heart defects or viability issues.
Conclusions:
- SHROOM3-associated heart defects do not originate from its loss within cardiomyocytes.
- Other cell types expressing SHROOM3, potentially cardiac neural crest cells, play a direct role in cardiac development.
- Further research is needed to elucidate the precise mechanisms and cell types involved.
