Vangl2-Regulated Polarisation of Second Heart Field-Derived Cells Is Required for Outflow Tract Lengthening during Cardiac Development

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Congenital heart defects are common, affecting almost 1% of all live births. Many of these affect the outflow region, where the aorta and pulmonary trunk connect with the main ventricular chambers. Congenital heart defects arise from disruption of normal developmental processes and can be modelled in mice. Thus, studying normal development, together with mouse mutants that develop heart malformations, should shed light on why these common anomalies arise. We have studied cardiac development in a mouse mutant for the Vangl2 gene, a key component of the planar cell polarity (PCP) pathway. This pathway controls the orientations of cells in epithelia and during directional cell migration. Here, we show that PCP signalling is required by cells derived from the second heart field, which forms the outflow tract walls. We show that in the absence of Vangl2, the cells within the distal outflow tract walls are non-polarised and disorganised. As a consequence the outflow tract is shortened and does not align properly with the ventricles. Thus, we show why disruption of a key PCP gene leads to outflow tract malformations. This is important for understanding heart development, but also more generally for understanding how PCP signalling regulates growth of tubular structures.

Vyšlo v časopise: Vangl2-Regulated Polarisation of Second Heart Field-Derived Cells Is Required for Outflow Tract Lengthening during Cardiac Development. PLoS Genet 10(12): e32767. doi:10.1371/journal.pgen.1004871
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1004871

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