Blocking MuRF1-mediated proteasome degradation preserves myofibril integrity in tre/ncx1 deficient hearts.
(A) Z-lines were visualized by α-actinin staining. By 72 hpf, sarcomeres are disassembled in hearts of uninjected (tre) and control morpholino-injected (tre +ctlMO) tremblor embryos. Murf1a/murf1 b knockdown does not affect sarcomere integrity in wild type embryos (WT +MO), but prevents sarcomere degradation in tre (tre +MO). Similarly, treatment with a proteasome inhibitor, MG132, preserves myofibril integrity in tre cardiomyocytes (tre +MG132). Scale bar, 10 μm. (B) Graph shows % of embryos with periodic α-actinin staining at 72 hpf. (C) Western blot detecting MuRF1 and β-actin proteins in uninjected control (WT control) and murf1a/murf1 b knockdown (MuRF1 MO) embryos. Chi-squared test, *p<0.05; **p<0.01; ***p<0.001.