A key difference between tetrapod limb buds and teleost fin buds is the presence of rigid actinotrichia fibers that guide migrating cells contributing to ray formation. Major structural components of actinotrichia are encoded by fish-specific actinodin (and) genes, which were lost in tetrapods. To investigate the consequences of this loss during the fin-to-limb transition, we generated deletions in zebrafish and1 and and2 using CRISPR/Cas9 mutagenesis. Double mutants (and1-/-and2-/-) lack actinotrichia. Embryos and larvae have reduced fin fold size, with disorganized cell migration. In adults, all fin fold-derived skeletal structures are disrupted, including the rays of all fins, as well as the caudal fin endoskeleton. Surprisingly, double mutant males fail to breed, despite being fertile. Video analysis revealed that males' fin defects impair their ability to stimulate egg release. Our findings highlight the role of actinotrichia in both fin patterning and in zebrafish courtship. We propose that actinodin gene maintenance is under strong selection in fish with similar courtship. We speculate that the loss of actinodin genes and a shift in courtship strategy may have coincided during tetrapod evolution.
Hanzelova et al. (Thu,) studied this question.