FIGURE

Fig 7

ID

ZDB-FIG-191230-641

Publication

Prill et al., 2019 - Myomesin is part of an integrity pathway that responds to sarcomere damage and disease

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Fig 7

Myomesin is absent in damaged skeletal muscle.

Zebrafish embryos treated with galanthamine (GAL) to induce muscle damage by hypercontraction from 28 to 48hpf demonstrated actin and myosin striations in both untreated (A&B) and treated (C&D) wild-type embryos; although GAL treated embryos exhibited fiber disorganization. Myomesin striations are visible in untreated wild-type embryos (E&F) while absent in GAL treated embryo muscle (G&H) even though actin striations, indicative of intact sarcomeres, are present (G’, white arrowheads; H’). qPCR analysis of ckmb and myom1a expression in galanthamine treated and untreated wild-type embryos demonstrated a significant decrease in the expression of both M-band genes at 48hpf (I). (Error bars are standard deviation. Expression is normalized using ef1a and wild-type at 48hpf).

Expression Data

Genes:	ckmb myom1a
Antibody:	Ab1-myom
Fish:	WT
Condition:	chemical treatment by environment: galanthamine
Anatomical Terms:	skeletal muscle cell whole organism
Stage:	Long-pec

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	WT
Condition:	chemical treatment by environment: galanthamine
Observed In:	skeletal muscle cell whole organism
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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