Author
Listed:
- Emily S. Noël
(Hubrecht Institute-KNAW and University Medical Center Utrecht)
- Manon Verhoeven
(Hubrecht Institute-KNAW and University Medical Center Utrecht)
- Anne Karine Lagendijk
(Hubrecht Institute-KNAW and University Medical Center Utrecht
Present address: Institute for Molecular Bioscience, University of Queensland, St Lucia, Queensland 4072, Australia)
- Federico Tessadori
(Hubrecht Institute-KNAW and University Medical Center Utrecht)
- Kelly Smith
(Hubrecht Institute-KNAW and University Medical Center Utrecht
Present address: Institute for Molecular Bioscience, University of Queensland, St Lucia, Queensland 4072, Australia)
- Suma Choorapoikayil
(Hubrecht Institute-KNAW and University Medical Center Utrecht
Present address: Université Montpellier II, 34095 Montpellier, Cedex 5, France)
- Jeroen den Hertog
(Hubrecht Institute-KNAW and University Medical Center Utrecht)
- Jeroen Bakkers
(Hubrecht Institute-KNAW and University Medical Center Utrecht
Interuniversity Cardiology Institute of the Netherlands)
Abstract
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.
Suggested Citation
Emily S. Noël & Manon Verhoeven & Anne Karine Lagendijk & Federico Tessadori & Kelly Smith & Suma Choorapoikayil & Jeroen den Hertog & Jeroen Bakkers, 2013.
"A Nodal-independent and tissue-intrinsic mechanism controls heart-looping chirality,"
Nature Communications, Nature, vol. 4(1), pages 1-9, December.
Handle:
RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3754
DOI: 10.1038/ncomms3754
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