Fig. 7

Functions of Hsp9 and Smarca4 are required for the blastema cell proliferation. (A–D) BrdU-incorporation in hspa9 mutants (A, C) and wild type sibling (B, D). Regeneration-dependent cell proliferation in response to amputation (double headed arrow in panel B) was apparently decreased in hspa9 mutants (A). Note that the regeneration-independent cell proliferation, in particular the cell proliferation at the caudal and ventral area, which gives rise to adult-type caudal fin (arrowheads in panels A–D), was also affected in this mutant (A, C). (E–H) BrdU-incorporation in yng/smarca4 mutants (E, F) and wild type sibling (G, H). Regeneration-dependent cell proliferation (double-headed arrows in panel F) was also apparently decreased in this mutant (E), but the regeneration-independent normal growth was only slightly affected (arrowheads in panels E–H). The same magnifications for panels A, B, E, F (scale bar in panel A) and panels C, D, G, H (scale bar in panel C). (I) Quantification of cell proliferation. Counting of BrdU-incorporated cells was carried out only in caudal fin fold (indicated by double-headed arrows) to exclude the regeneration-independent cell proliferation. Data in the graph are the mean ± SEM. Statistical significance was tested by Student's t-test. *P < 0.01. (J, K) BrdU incorporation in the trunk regions of yng/smarca4 mutants (J) and wild type sibling (K). BrdU incorporation in yng/smarca4 mutants was indistinguishable from that of wild type siblings in other body regions, suggesting that the mutants have no apparent defect in normal cell proliferation.