Abstract:

Ｏｂｊｅｃｔｉｖｅ：In this study,we chose zebrafish as our model organism and constructed TYRO3 homozygous mutant which was helpful to explore change of its function caused by TYRO3 knockout using CRISPR/Cas9 system.
Ｍｅｔｈｏｄｏｌｏｇｙ：PCR and sequencing were used to identify the mutations in the embryo.The effects of TYRO3 mutants on zebrafish edema were observed,as well as foot process effacement visualizing by transmission electron microscopy.
Ｒｅｓｕｌｔｓ：We got two frameshift TYRO3 mutants，2 and 5 homozygous for each TYRO3 mutants were acquired in F2.Heterozygous rate was 50% in F0.TYRO3 mutants lead to impaired glomerular filtration barrier(GFB),as presented by pericardial and periorbital edema,and podocyte footprocess effacement.
Ｃｏｎｃｌｕｓｉｏｎ：We successfully constructed a homozygous zebrafish with gene TYRO3 knockout and preliminarily confirmed that TYRO3 deletion could cause damage to zebrafish podocytes injury.

Key words: TYRO3 receptor tyrosine kinase, CRISPR/Cas9, zebrafish