ArticleCardiovascular research2014
Scrib:Rac1 interactions are required for the morphogenesis of the ventricular myocardium.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Exploration of candidate genes associated with rare SNVs in pulmonary stenosis using whole-exome sequencing and machine learning.Frontiers in genetics · 2026Article
- Establishment and functional studies of a model of cardiomyopathy with cardiomyocyte-specific conditional knockout of Arhgef18.Disease models & mechanisms · 2025Article
- Scribble basal polarity acquisition in RPE cells and its mislocalization in a pathological AMD-like model.Frontiers in neuroanatomy · 2022Article
- Neuron-Specific Deletion ofFrontiers in genetics · 2022Article
- On the PHLPPside: Emerging roles of PHLPP phosphatases in the heart.Cellular signalling · 2021Review
- Myocardium-Specific Deletion of Rac1 Causes Ventricular Noncompaction and Outflow Tract Defects.Journal of cardiovascular development and disease · 2021Article
- Llgl1 regulates zebrafish cardiac development by mediating Yap stability in cardiomyocytes.Development (Cambridge, England) · 2020Article
- Alternative splicing of jnk1a in zebrafish determines first heart field ventricular cardiomyocyte numbers through modulation of hand2 expression.PLoS genetics · 2020Article
- A Novel Heterozygous Variant in F2 Gene in a Chinese Patient With Coronary Thrombosis and Acute Myocardial Infarction Leads to Antithrombin Resistance.Frontiers in genetics · 2020Article
- Novel mouse model of encephalocele: post-neurulation origin and relationship to open neural tube defects.Disease models & mechanisms · 2019Article
- AFrontiers in pediatrics · 2019Article
- Disruption of Planar Cell Polarity Pathway Attributable to Valproic Acid-Induced Congenital Heart Disease through Hdac3 Participation in Mice.Chinese medical journal · 2018Article
- Development and maturation of the fibrous components of the arterial roots in the mouse heart.Journal of anatomy · 2018Article
- Noncompaction cardiomyopathy and heterotaxy syndrome.Progress in pediatric cardiology · 2017Article
- Re-evaluation of hypoplastic left heart syndrome from a developmental and morphological perspective.Orphanet journal of rare diseases · 2017Article
- Cilia and Ciliopathies in Congenital Heart Disease.Cold Spring Harbor perspectives in biology · 2017Review
- Nkx2-5 and Sarcospan genetically interact in the development of the muscular ventricular septum of the heart.Scientific reports · 2017Article
- APT2 Inhibition Restores Scribble Localization and S-Palmitoylation in Snail-Transformed Cells.Cell chemical biology · 2017Article
- Prickle1 mutation causes planar cell polarity and directional cell migration defects associated with cardiac outflow tract anomalies and other structural birth defects.Biology open · 2016Article
- Vangl2-regulated polarisation of second heart field-derived cells is required for outflow tract lengthening during cardiac development.PLoS genetics · 2014Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
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Abstract
aimsThe organization and maturation of ventricular cardiomyocytes from the embryonic to the adult form is crucial for normal cardiac function. We have shown that a polarity protein, Scrib, may be involved in regulating the early stages of this process. Our goal was to establish whether Scrib plays a cell autonomous role in the ventricular myocardium, and whether this involves well-known polarity pathways. METHODS AND
resultsDeletion of Scrib in cardiac precursors utilizing Scrib(flox) mice together with the Nkx2.5-Cre driver resulted in disruption of the cytoarchitecture of the forming trabeculae and ventricular septal defects. Although the majority of mice lacking Scrib in the myocardium survived to adulthood, they developed marked cardiac fibrosis. Scrib did not physically interact with the planar cell polarity (PCP) protein, Vangl2, in early cardiomyocytes as it does in other tissues, suggesting that the anomalies did not result from disruption of PCP signalling. However, Scrib interacted with Rac1 physically in embryonic cardiomyocytes and genetically to result in ventricular abnormalities, suggesting that this interaction is crucial for the development of the early myocardium.
conclusionsThe Scrib-Rac1 interaction plays a crucial role in the organization of developing cardiomyocytes and formation of the ventricular myocardium. Thus, we have identified a novel signalling pathway in the early, functioning, heart muscle. These data also show that the foetus can recover from relatively severe abnormalities in prenatal ventricular development, although cardiac fibrosis can be a long-term consequence.
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