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Fig. 6 Genetic mutations affecting the larval fin fold regeneration. (A, B) Disrupted larval fin fold regeneration in hspa9 mutants. The larval regeneration was apparently impaired (severe defect in 44/56 mutants, mild defect in 8/56 mutants; (A), whereas the uncut mutants did not show such defects (B). (C, D) Disrupted larval fin fold regeneration in yng/smarca4 mutants. A complete penetrance of defect in regeneration was observed in yng/smarca4 mutants (n = 28/28 mutants, C). Despite the mutant phenotypes such as smaller eyes and curved body axis, hspa9 and yng/smarca4 mutants were alive at 5 dpf and retain a good cellular viability. (E, F) Normal regeneration in other mutants. Several other mutants including you mutants, which have a defect in hedgehog signaling (Kawakami et al., 2005), did not display such defects (n = 15, E). The same magnifications for panels A–F (scale bar in panel A).
Reprinted from Developmental Biology, 325(1), Yoshinari, N., Ishida, T., Kudo, A., and Kawakami, A., Gene expression and functional analysis of zebrafish larval fin fold regeneration, 71-81, Copyright (2009) with permission from Elsevier. Full text @ Dev. Biol.