Figure 9.
Figure 9. Dysferlin and myoferlin contribute to plasma membrane repair. Myofibers from dysferlin-null (Dysf), myoferlin-null (Myof), Dysf/Myof double-null (FER), and wild-type (WT) animals were isolated and subjected to laser-induced injury in the presence of FM1-43 fluorescence. Similar to FM4-64, FM1-43 is a lipophilic dye that increases fluorescence as it binds damaged membrane (Zweifach, 2000; Yeung et al., 2009). (A) Representative images are shown demonstrating FM1-43 uptake after injury. (B and C) Both Dysf and Myof fibers had increased FM1-43 uptake compared with wild type (*, P < 0.05). FER animals, lacking both Dysf and Myof, had significantly more FM1-43 dye uptake than either single mutant, consistent with a compensatory role of ferlin proteins (**, P < 0.01; n = 6 myofibers from n = 2 mice per genotype). Bars, 4 µm. Error bars represent SEM.

Dysferlin and myoferlin contribute to plasma membrane repair. Myofibers from dysferlin-null (Dysf), myoferlin-null (Myof), Dysf/Myof double-null (FER), and wild-type (WT) animals were isolated and subjected to laser-induced injury in the presence of FM1-43 fluorescence. Similar to FM4-64, FM1-43 is a lipophilic dye that increases fluorescence as it binds damaged membrane (Zweifach, 2000; Yeung et al., 2009). (A) Representative images are shown demonstrating FM1-43 uptake after injury. (B and C) Both Dysf and Myof fibers had increased FM1-43 uptake compared with wild type (*, P < 0.05). FER animals, lacking both Dysf and Myof, had significantly more FM1-43 dye uptake than either single mutant, consistent with a compensatory role of ferlin proteins (**, P < 0.01; n = 6 myofibers from n = 2 mice per genotype). Bars, 4 µm. Error bars represent SEM.

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