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Fig. 4 Col9α1 morpholino phenocopies the prp finfold phenotype while overexpression of col9α1 rescues prp. (A) A gene-specific morpholino (MO) targeting the splice site of col9α1 exon 5 caused the small-finfold phenotype in wild-type (WT) embryos. (B) The tail of a 2-day post-fertilization (dpf) uninjected WT embryo showing a normal finfold with radial actinotrichia (arrow). (C) A prp embryo showing a small finfold with short and sparse actinotrichia (arrow). (D) A WT embryo injected with the col9α1 MO developed the prp-like small-finfold and actinotrichia defects. (E) A prp embryo injected with the col9α1 plasmid developed a mosaic finfold with a prp-like portion in the dorsal half and a normal-looking portion in the ventral half where normal actinotrichia can be seen (arrow). Arrows, actinotrichia. Anterior, left; dorsal top.
Reprinted from Developmental Biology, 332(2), Huang, C.C., Wang, T.C., Lin, B.H., Wang, Y.W., Johnson, S.L., and Yu, J., Collagen IX is Required for the Integrity of Collagen II Fibrils and the Regulation of Vascular Plexus Formation in Zebrafish Caudal Fins, 360-370, Copyright (2009) with permission from Elsevier. Full text @ Dev. Biol.