Key result
Exposure to cytochalasin D (5 nM-2.0 microM) and latrunculin A (25 nM-2.0 microM) suppressed cardiac c-looping in stage 9-11 chick embryos in a stage- and concentration-dependent manner.
Ongoing actin polymerization is required for the bending component of cardiac c-looping during early embryonic heart development.
No immediate clinical implications; leaves open actin’s role in human cardiac looping pending mammalian validation.
During cardiac c-looping, the heart transforms from a straight tube into a c-shaped tube, presenting the first evidence of left-right asymmetry in the embryo. C-looping consists of two primary deformation components: ventral bending and dextral rotation. This study examines the role of actin polymerization in bending of the heart tube. Exposure of stage 9-11 chick embryos to low concentrations of the actin polymerization inhibitors cytochalasin D (5 nM-2.0 microM) and latrunculin A (LA; 25 nM-2.0 microM) suppressed looping in a stage- and concentration-dependent manner in both whole embryos and isolated hearts. Local exposure of either the dorsal or ventral sides of isolated hearts to LA also inhibited looping, but less than global exposure, indicating that both sides contribute to the bending mechanism. Taken together, these data suggest that ongoing actin polymerization is required for the bending component of cardiac c-looping, and we speculate that polymerization-driven myocardial cell shape changes cause this deformation.
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Latacha et al. (2005) studied Cardiac c-looping. Actin polymerization inhibitors (cytochalasin D and latrunculin A) was evaluated on Suppression of cardiac looping. Exposure to cytochalasin D (5 nM-2.0 microM) and latrunculin A (25 nM-2.0 microM) suppressed cardiac c-looping in stage 9-11 chick embryos in a stage- and concentration-dependent manner.
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