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Figure 8. Ctnnd1 knockouts in Xenopus give rise to altered morphogenesis of the muscles and heart. (A) Immunofluorescent staining for collagen 2 (col2, magenta), muscle/pax2 (white) and nuclei (DAPI, blue); (a, anterior; p, posterior; d, dorsal; v, ventral). (A) (a, e) A lateral view of col2-positive branchial cartilages in UIC (a) and p120 CRISPR mutant (e) reveals the hypoplasia of mutant cartilages; however, cell morphology appears normal in p120 CRISPR mutants (h) (d and h, white arrowheads). (A) (b, c, f and g) Pax2-expressing muscles revealed a defect in the fibril organization of the rectus abdominus muscle in the p120 CRISPR tadpoles (f, white arrowhead) compared with the UIC muscles (b, white arrowhead); note insets in (c, g). (B) Ventral views of hearts of stage 46 tadpoles. Immunofluorescent staining for p120-catenin (green), E-cadherin (red) and DNA (blue). (B) (i–m) Controls; (n–r) p120 CRISPR mutant tadpoles. Morphologic defects are evident in the size of the heart and directionality of the loops (compare control heart (i) to mutant heart (n), yellow-dashed outlines). (B) (k, p) p120-catenin is strongly expressed in the heart of UIC tadpoles (k) but is lost in p120 CRISPR tadpoles (p). (B) (l, q) Note the absence of E-cadherin in the control and mutant hearts. Scale bars = 100 μm. |
