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Muscle and neuron specific Smn RNAi knockdown causes NMJ defects.

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posted on 15.09.2008 by Howard Chia-Hao Chang, Douglas N. Dimlich, Takakazu Yokokura, Ashim Mukherjee, Mark W. Kankel, Anindya Sen, Vasanthi Sridhar, Tudor A. Fulga, Anne C. Hart, David Van Vactor, Spyros Artavanis-Tsakonas

(A–I) Reduced SMN expression in the N4, C24 and FL26B UAS-Smn-RNAi transgenic constructs elicits graded effects on NMJ morphology using the ubiquitous actinGAL4 (A, D, G) as well as the tissue-specific how24BGAL4 (muscle) (B, E, H) and elavGAL4 (neuron) (C, F, I) drivers. Vector only (pWIZ) controls are shown (J, K, L). In these images the pre- and post-synaptic tissues are labeled with antibodies against Synaptotagmin (green) and Discs large (red), respectively. (M) Bouton counts for the NMJs from the genotypes shown in (A–L) were normalized for muscle area and subtracted from vector only controls. For each genotype at least 15 animals were examined. * P<0.01 and **P<0.05 was determined by the ANOVA multiple comparisons test. Scale bars represent 15 µm.

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