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Article Abstract
To elucidate the control mechanism of tail resorption during metamorphosis, the expression of , a macrophage-apoptotic cell bridging molecule that promotes phagocytosis in mammals, was examined. In both and , the expression in the tail increased significantly during metamorphosis, reaching its peak at the metamorphic climax, when the tail shortens rapidly. This finding suggests that the up-regulation of at metamorphic climax is involved in the clearance of apoptotic tail muscles. To investigate the significance of up-regulation, -deficient tadpoles were generated using the CRISPR/Cas9 method, and the effects of -deletion were examined. Delayed tail resorption process was observed in the -deficient mutants (from 9.8 days [wild type] to 13.2 days [F2 mutant]), suggesting that elevated expression during the metamorphic climax contributes to the tail resorption.
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