Defective sarcomere assembly in and zebrafish mutants.

Two paralogues, and have been identified in zebrafish. Although Smyd1b function has been reported in fast muscle, its function in slow muscle and the function of Smyd1a, in general, are uncertain. In this study, we generated 2 mutant alleles and analyzed the muscle defects in and single and double mutants in zebrafish. We demonstrated that knockout of alone had no visible effect on muscle development and fish survival. This was in contrast to the mutant, which exhibited skeletal and cardiac muscle defects, leading to early embryonic lethality. The and double mutants, however, showed a stronger muscle defect compared with or mutation alone, namely, the complete disruption of sarcomere organization in slow and fast muscles. Immunostaining revealed that double mutations had no effect on myosin gene expression but resulted in a dramatic reduction of myosin protein levels in muscle cells of zebrafish embryos. This was accompanied by the up-regulation of and gene expression. Together, our studies indicate that both Smyd1a and Smyd1b partake in slow and fast muscle development although Smyd1b plays a dominant role compared with Smyd1a.-Cai, M., Han, L., Liu, L., He, F., Chu, W., Zhang, J., Tian, Z., Du, S. Defective sarcomere assembly in and zebrafish mutants.