Abstract
Many organs in vertebrates are left-right asymmetrical located. For example, liver is at the right side and stomach is at the left side in human. Fibroblast growth factor (Fgf) signaling is important for left-right asymmetry. To investigate the roles of Fgfr2 signaling in zebrafish left-right asymmetry, we used splicing blocking morpholinos to specifically block the splicing of fgfr2b and fgfr2c variants, respectively. We found that the relative position of the liver and the pancreas were disrupted in fgfr2c morphants. Furthermore, the left-right asymmetry of the heart became random. Expression pattern of the laterality controlling genes, spaw and pitx2c, also became random in the morphants. Furthermore, lefty1 was not expressed in the posterior notochord, indicating that the molecular midline barrier had been disrupted. It was also not expressed in the brain diencephalon. Kupffer's vesicle (KV) size became smaller in fgfr2c morphants. Furthermore, KV cilia were shorter in fgfr2c morphants. We conclude that the fgfr2c isoform plays an important role in the left-right asymmetry during zebrafish development.
Highlights
The bodies of most adult animals have left-right symmetry
We found that the orientation of asymmetric organs was randomized after knocking down Fibroblast Growth Factor Receptor 2 (Fgfr2)
These results suggest that fgf8, fgf24, and fgfr1 are important for ciliogenesis
Summary
The bodies of most adult animals have left-right symmetry. Mechanisms involved in the regulation of laterality for various animal species have been identified. These include motor proteins, ion channel, cytoskeleton, serotonin, cell-cell junction, Ca2+, and cilia [3]. In the mouse, the leftward movement of fluid at the ventral node, called nodal flow, is the critical process for left-right asymmetry [4]. The nodal flow is generated by the clockwise rotation of nodal cilia. This directional flow causes some morphogens to concentrate at left side of the node and leads to left-right polarization [5,6]
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