Fish skeletal muscle is rich in mitochondria， especially in red muscle fibers. Mitochondria play an important role in maintaining the contraction of fish skeletal muscle. Tafazzin （taz） gene， as an important gene for the synthesis of mitochondrial-specific phospholipid cardiolipin， plays a key role in the production of mitochondrial ATP. Through in situ hybridization of zebrafish muscle tissue sections， the results showed the taz gene was expressed in zebrafish skeletal muscle， and specifically expressed in the I zone of myofibrils. The taz^-/- mutant was further constructed in zebrafish by CRISPR/Cas9 technology， and it was found that after taz deletion， the body length， weight， body width， and height of taz^-/- were significantly smaller than wild-type zebrafish （P<0.05）. It shows that mutation of taz gene lead to growth and developmental delay in zebrafish. The fluorescence staining of 48 hpf embryos showed that the muscle fibers from the taz^-/- mutant was looser than WT. Statistical analysis of F-actin length showed that the H-H length of taz^-/- was（1.12±0.03）μm， while the wild-type zebrafish H-H length was（0.59±0.01）μm， indicating that the length of actin was significantly longer （P<0.05）. Whole Alizarin stain of zebrafish showed the length of intermuscular bones became smaller in taz^-/- than WT. The above results indicate that taz affects the growth， actin contraction and ossification of intermuscular bones.