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Fig. 7

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ZDB-IMAGE-140416-6
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Figures for Myhre et al., 2014
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Fig. 7 Stress-responsive gene expression is not increased in hel mutant embryos during early myofibrillogenesis. Expression of myosin folding stress-responsive genes hsp90a1 (A–D) and unc45b (E–H) did not change in hel mutant embryos (C and D and G and H) when compared with wild-type controls (A and B and E and F). Increased mRNA expression of stress-responsive genes was assessed by in situ hybridization at 24 (left) and 36 hpf (right). At 24 hpf, when increased expression of myosin chaperones is expected in mutants with myosin assembly defects, no qualitative change could be detected between WT and hel mutant embryos for either gene (compare A with C and E with G). Even at 36 hpf, expression was not greatly increased (compare B with D and F with H), although the extent of mRNA expression in the tail somites was somewhat greater in mutants (arrows). There was little variability between individuals within experimental groups from two independent experiments (n=20 embryos per group).

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Reprinted from Developmental Biology, 387(1), Myhre, J.L., Hills, J.A., Prill, K., Wohlgemuth, S.L., and Pilgrim, D.B., The titin A-band rod domain is dispensable for initial thick filament assembly in zebrafish, 93-108, Copyright (2014) with permission from Elsevier. Full text @ Dev. Biol.