Li, H., Zhong, Y., Wang, Z., Gao, J., Xu, J., Chu, W., Zhang, J., Fang, S., and Du, S.J. (2013) Smyd1b is required for skeletal and cardiac muscle function in zebrafish. Molecular biology of the cell. 24(22):3511-21.
Smyd1b is a member of the Smyd family, which is specifically expressed in skeletal and cardiac muscles. Smyd1b plays a key
role in thick filament assembly during myofibrillogenesis in skeletal muscles of zebrafish embryos. To better characterize
Smyd1b function and its mechanism of action in myofibrillogenesis, we have analyzed the effects of smyd1b knockdown on myofibrillogenesis in skeletal and cardiac muscles of zebrafish embryos. The results showed that knockdown of
smyd1b caused a significant disruption of myofibril organization in both skeletal and cardiac muscles of zebrafish embryos. Microarray
and quantitative RT-PCR analyses showed that knockdown of smyd1b upregulated heat shock protein 90 (hsp90) and unc45b gene expression. Biochemical analysis revealed that Smyd1b could be coimmunoprecipitated with Hsp90α1 and Unc45b, two myosin
chaperones expressed in muscle cells. Consistent with its potential function in myosin folding and assembly, knockdown of
smyd1b significantly reduced myosin protein accumulation without affecting their mRNA expression. This likely resulted from increased
myosin degradation involving unc45b overexpression. Together, these data support the idea that Smyd1b may work together with myosin chaperones to control myosin
folding, degradation and assembly into sarcomeres during myofibrillogenesis.