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Molecular asymmetries in actin dynamics drive left‐right organogenesis
Author(s) -
Trinh Le A.,
Koo Eun,
Trivedi Vikas,
Bagnat Michel,
Fraser Scott E.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.228.1
Subject(s) - morphogenesis , zebrafish , actin , organogenesis , microbiology and biotechnology , lateral plate mesoderm , nodal , biology , anatomy , mesoderm , live cell imaging , actin cytoskeleton , dynamics (music) , myosin , cytoskeleton , embryonic stem cell , physics , genetics , cell , gene , acoustics
The embryonic heart tube arises from bilaterally symmetric populations of cells in the anterior lateral plate mesoderm (LPM). These bilateral progenitors undergo epithelial maturation and migrate as coherent sheets of cells that fuse at the midline to form the linear heart tube, which exhibit left‐right asymmetry. Here, we explore the dynamics of the actin cytoskeleton in coordinating the morphogenesis of the LPM during heart tube formation in zebrafish using a fluorescent reporter of actin dynamics, LifeAct‐GFP. Multiphoton time‐lapse microscopy coupled with quantitative analysis of 4‐dimensional data (x,y,z,t) reveal a number of dynamics in actin polymerization within the LPM that is suggestive of differential force exertion from the LPM cells as they undergo morphogenesis. These actin dynamics are asymmetrically distributed and are dependent on both Nodal signaling and tissue‐tissue interaction. The asymmetries can be uncoupled genetically and are required for leftward placement of the heart tube. Taken together, these data suggest that the LPM exerts multiple cellular traction forces as it undergoes midline migration and morphogenesis to form a leftward positioned linear heart tube.

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