myf5基因對斑馬魚頭部發育之功能分析
Roles of Myf5 During Craniofacial Developmnt in Zebrafish
Date Issued
2006
Date
2006
Author(s)
Lin, Cheng-Yung
DOI
en-US
Abstract
The myogenic regulatory factor Myf5 is well known as a fundamental molecule to trunk myogenesis. However, little is known about the role that myf5 plays in craniofacial development. We observed that zebrafish myf5 was detected in the primordia of the obliques, lateral rectus, sternohyoideus, and pharyngeal mesoderm cores. In contrast, myod transcripts were expressed in all head muscle precursors at later stages. Knockdown of myf5 revealed that Myf5 was required for the development of the obliques, lateral rectus, sternohyoideus, and all pharyngeal muscles, whereas knockdown of myod proved that Myod was required for the development of superior rectus, medial rectus, inferior rectus, lateral rectus, and the ventral pharyngeal muscles. myod mRNA did not rescue the loss of the cranial muscle caused by injecting myf5-morpholino, or vice versa, suggesting that the functions of Myf5 and Myod were not redundant in head paraxial mesoderm, a finding different from their functions in trunk myogenesis. Myf5, but not Myod, was required for the forward migration of myf5-positive oblique precursors. All evidences reveal that Myf5 and Myod function independently during cranial myogenesis. On the basis of the expression patterns of myf5 and myod, we propose a model to present how Myf5 and Myod are involved in head myogenesis of zebrafish.
We show that Myf5 knockdown in zebrafish results in abnormal development of cranial cartilage. The expression of neural crests markers was dramatically reduced in the myf5 morphants. The TUNEL assay showed that apoptosis occurred significantly in the head of the myf5 morphants. Of interest, the pharyngeal arch defects found in the myf5 morphants were identical to those of the fgf3-morpholino(MO)-injected embryos, and the expression of fgf3 and its down-regulators erm and pea3 was greatly reduced in the myf5 morphants. We proved that the segmentation of the hindbrain were affected severely in the myf5 morphants due to either lost or defective expression of krox20 and pax6, indicating that the defects in the crest and arch were attributable to the disordered hindbrain segmentation. The fgf3 transcripts also were reduced in the myf5 morphants, but co-injection of fgf3 mRNA and myf5-MO1 into the embryos rescued the hindbrain patterning and the ceratobranchial cartilage defects; the apoptotic signals were also reduced. This evidence suggests that myf5 directs fgf3 signaling to mediate hindbrain development. We observed that myf5 was expressed in the non-axial mesoderm at the shield stage. Knockdown of Myf5 resulted in abnormal expansion and disorder of the dorsal organizer, which caused the defective hindbrain, crest, and cartilage development. Therefore, we propose that Myf5 plays roles in the development of the hindbrain boundary, cranial neural crest, and pharyngeal cartilage.
Subjects
斑馬魚
頭部發育
基因調控
胚胎發育
myf5
zebrafish
craniofacial development
gene regulation
Type
other
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