期刊
JOURNAL OF CELL BIOLOGY
卷 181, 期 2, 页码 381-394出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200708022
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资金
- NCI NIH HHS [R01 CA039481, R01 CA47282, R01 CA39481, R01 CA120975, R01 CA047282] Funding Source: Medline
- NIAAA NIH HHS [T32 AA007463, T32 AA07463] Funding Source: Medline
Perlecan's developmental functions are difficult to dissect in placental animals because perlecan disruption is embryonic lethal. In contrast to mammals, cardiovascular function is not essential for early zebrafish development because the embryos obtain adequate oxygen by diffusion. In this study, we use targeted protein depletion coupled with protein-based rescue experiments to investigate the involvement of perlecan and its C-terminal domain V/endorepellin in zebrafish development. The perlecan morphants show a severe myopathy characterized by abnormal actin. lament orientation and disorganized sarcomeres, suggesting an involvement of perlecan in myopathies. In the perlecan morphants, primary intersegmental vessel sprouts, which develop through angiogenesis, fail to extend and show reduced protrusive activity. Live video-microscopy confirms the abnormal swimming pattern caused by the myopathy and anomalous head and trunk vessel circulation. The phenotype is partially rescued by micro-injection of human perlecan or endorepellin. These findings indicate that perlecan is essential for the integrity of somitic muscle and developmental angiogenesis and that endorepellin mediates most of these biological activities.
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