Abstract
Sox9 is a multifunctional gene and plays crucial roles in vertebrate development including chondrogensis. In teleost, due to the genome duplication event, there are two co-orthologs sox9a and sox9b. In this study, CRISPR/Cas9 technology was performed to disrupt the function of either sox9a or sox9b. All sox9a mutants (sox9aΔ10 and sox9aΔ67) and sox9b mutants (sox9bΔ11 and sox9bΔ20) lost HMG domain and Q/S domain, however, only sox9a mutant larvae had mis-shaped pectoral fins and lacked the scapulocoracoid cartilage. sox9b mutant larvae showed normal cartilages similar to wild type larvae. The results suggested that sox9a, not sox9b was required for cartilage development in zebrafish, which was different from the sox9b-mutant phenotype induced by N-ethyl-N-nitrosourea (ENU) treatment, gamma radiation treatment or morpholino injection. This study confirmed that ancestral sox9 gene functions partitioned between the two paralogs in zebrafish.
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