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. 2015 Nov 16;10(11):e0142836. doi: 10.1371/journal.pone.0142836

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© 2015 Novak et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 1 — (A) Western blot analysis showing the complete knockout of dFmr1 (dFmr1 ^3/50M) compared to wild type (w ¹¹¹⁸) and genomic rescue (P[dFmr1]/+; dFmr1 ^3/50M). (B) Loss of dFmr1 (dFmr1 ^3/50M, N = 16) results in a statistically significant decrease in heart rate when compared to wild type (w ¹¹¹⁸, N = 10). This is rescued by expression of a wild type copy of dFmr1 in its genomic context (P[dFmr1]/+; dFmr1 ^3/50M, N = 10). (C) Western blot showing that two independent RNAi lines (24B Gal4> dFmr1 ^RNAi-2, dFmr1 ^RNAi-2) result in almost complete striated muscle-specific knockdown of dFMR1 (i.e., ~85–100%) compared to control (24B Gal4> w ¹¹¹⁸). (D) Pan-muscle (24B Gal4) RNAi knockdown of dFmr1 (24B Gal4> dFmr1 ^RNAi-1, N = 12 and dFmr1 ^RNAi-2, N = 6) leads to a significant decrease in heart rate compared to control (24B Gal4> w ¹¹¹⁸, N = 17). Student’s T-test was used to calculate statistical significance: p values, * <0.05, ** <0.01, **** <0.0001.