Skip to main content
Fig. 2 | Translational Neurodegeneration

Fig. 2

From: Impaired dynamic interaction of axonal endoplasmic reticulum and ribosomes contributes to defective stimulus–response in spinal muscular atrophy

Fig. 2

Overexpression of either SMN or actin rescues the impaired axonal ER dynamics in Smn-deficient motoneurons. a Motoneurons that were transduced with pSIH-GFP-SMN or pSIH-GFP lentiviruses were identified via GFP expression. b Representative time lapse images of ER movements in growth cone filopodia of Smn+/+;SMN2tgtg neurons co-expressing GFP and mCherry-ER (WTCtrl), Smn−/−;SMN2tgtg neurons co-expressing GFP and mCherry-ER (KOCtrl), Smn−/−;SMN2tgtg neurons co-expressing GFP-SMN and mCherry-ER (KOrescue−SMN) and Smn−/−;SMN2tgtg neurons co-expressing GFP-actin and mCherry-ER (KOrescue−actin). c ER dynamics are higher in growth cone filopodia of KOrescue−SMN compared to the KOCtrl group (**P = 0.0016 for WTCtrl vs. KOCtrl; **P = 0.0011 for KOCtrl vs. KOrescue−SMN; n = 22–26 cells from 3 independent experiments). ER dynamics are increased in filopodia of KOrescue−actin motoneurons compared to the KOCtrl group (*P = 0.0468; n = 12–26 filopodia from 3 independent experiments). All data are normalized to WTCtrl control. Data are presented in scatter dot plot; error bars represent mean ± SEM. Statistical analyses were done by One-way ANOVA with Dunn’s post-hoc test

Back to article page