Fig. 2: Mbl RNAi suppresses neuromuscular junction defects and motor dysfunction. | Nature Communications

Fig. 2: Mbl RNAi suppresses neuromuscular junction defects and motor dysfunction.

From: Muscleblind acts as a modifier of FUS toxicity by modulating stress granule dynamics and SMN localization

Fig. 2: Mbl RNAi suppresses neuromuscular junction defects and motor dysfunction.The alternative text for this image may have been generated using AI.

Neuronal expression of wild-type and ALS-linked mutants of FUS cause defects in larval neuromuscular junction (NMJ) morphology and motor dysfunction, both of which are rescued by knockdown of endogenous Mbl. Tissue-specific expression of FUS in the motor neurons (D42-gal4) of third-instar larvae causes morphological defects of NMJs at muscle 4 from segments A2–A5. a Immunofluorescence images of NMJs using presynaptic (HRP) and postsynaptic (DLG) markers. Scale bars = 10 µm. The average number b and size of mature boutons d are unaffected by FUS expression. c Expression of FUS in motor neurons results in an aberrant increase satellite bouton numbers (white arrows), which is significantly rescued by knockdown of endogenous Mbl. (N > 25 NMJs from > 8 animals were used for analyses). Values in b and c are represented as the mean ± SEM. Statistical comparisons in b–d were determined using one-way ANOVA with Tukey’s multiple comparisons test for each FUS group (*P < 0.05, **P < 0.01, ****P < 0.0001, NS = not significant). Comparisons between control and mbl RNAi groups were performed with unbalanced t tests. e Quantification of the percent of adult flies that climb up to 10 centimeters. Values are represented as the mean ± SD. (N > 50 flies with data were collected in triplicate). Statistical comparisons were performed on GraphPad Prism using one-way ANOVA with Tukey’s multiple comparisons test for each FUS group.

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