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. 2017 Aug 28;13(8):e1006968. doi: 10.1371/journal.pgen.1006968

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© 2017 Ulian-Benitez 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 credited.

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Fig 10 — Confocal images showing A3-4 muscle 6/7 NMJs, labeled as in Fig 9. (A) Reduced pCaMKII^T287 levels in kek-6 mutants, and kek-6 DNT2 double mutants. Kurskal-Wallis p = 0.0009, and post-hoc Dunn. (B-D) Over-expresison of activated CaMKII^T287D in motoneurons rescued the NMJ phenotypes of (B) kek-6 mutants, Kruskal-Wallis p = 0.0081, post-hoc Dunn; (C) DNT2 mutants, Kruskal-Wallis p = 0.0001, post-hoc Dunn, and (D) kek-6 DNT2 double mutants. Welch ANOVA p<0.000, post-hoc Games-Howell. *p<0.05, **p<0.01, ***p<0.001 see S1 Table. N = 23–75 hemisegments. Genotypes: MN = motoneurons, D42GAL4; Neurons: elavGAL4. Different neuronal drivers were used due to genetic constraints. Control: wild-type: yw/+; grey boxes: D42GAL4/+. (A) Mutant genotypes as in Fig 4; Rescues: (B) w;UASCaMKII^T287D/+; D42GAL4 kek6³⁴/ Df(3R)6361. (C) w;UASCaMKII^T287D/+; elavGAL4 Df(3L)6092/DNT2³⁷. (D) w; UASCaMKII^T287D/Toll-7GAL4; kek6³⁴Df(3L)6092/ Df(3R)6361 DNT2³⁷.