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A Nodal-independent and tissue-intrinsic mechanism controls heart-looping chirality
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A Nodal-independent and tissue-intrinsic mechanism controls heart-looping chirality
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Journal Article
A Nodal-independent and tissue-intrinsic mechanism controls heart-looping chirality
2013
Overview
Breaking left–right symmetry in bilateria is a major event during embryo development that is required for asymmetric organ position, directional organ looping and lateralized organ function in the adult. Asymmetric expression of Nodal-related genes is hypothesized to be the driving force behind regulation of organ laterality. Here we identify a Nodal-independent mechanism that drives asymmetric heart looping in zebrafish embryos. In a unique mutant defective for the Nodal-related
southpaw
gene, preferential dextral looping in the heart is maintained, whereas gut and brain asymmetries are randomized. As genetic and pharmacological inhibition of Nodal signalling does not abolish heart asymmetry, a yet undiscovered mechanism controls heart chirality. This mechanism is tissue intrinsic, as explanted hearts maintain
ex vivo
retain chiral looping behaviour and require actin polymerization and myosin II activity. We find that Nodal signalling regulates actin gene expression, supporting a model in which Nodal signalling amplifies this tissue-intrinsic mechanism of heart looping.
Nodal signalling has been implicated in the asymmetric positioning of various organs. Here, Noël
et al.
show that the asymmetry of the embryonic zebrafish heart is also established in the absence of Nodal signalling, suggesting a Nodal-independent mechanism that relies on actomyosin activity.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 45/70
/ 45/77
/ 631/136
/ 631/67
/ 64/116
/ Animals
/ Body Patterning - physiology
/ Embryo, Nonmammalian - anatomy & histology
/ Embryo, Nonmammalian - physiology
/ Embryos
/ Gene Expression Regulation, Developmental - physiology
/ Humanities and Social Sciences
/ Mutation
/ Science
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