Journal: Nature Communications
Article Title: Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease
doi: 10.1038/s41467-017-00689-z
Figure Lengend Snippet: Depletion of Plekhg5 results in axon growth defects and degeneration of axon terminals in vitro. a Motoneurons were transduced with sh-control or sh-Plekhg5 #D lentiviruses or left untreated. Scale bar : 100 µm. b Seven days after sh-RNA transduction, knockdown of Plekhg5 reduced axon length, whereas dendrite length and number of dendrites were not affected. Each data point represents the mean of one individual experiment with at least 20 cells analyzed. One-way ANOVA, Bonferroni post-test. c – e Motoneurons were cultured for seven days and stained for synaptophysin, Rab26 and F-actin and imaged by confocal c and SIM microscopy e . c Scale bar : 10 µm. d Quantification of axon terminal size ( n = 15 cells; unpaired t -test; two-tailed). e Motoneurons were cultured for 7 days and stained for synaptophysin, Rab26 and F-actin and imaged by SIM microscopy. Axons of Plekhg5 −/− motoneurons display synaptophysin positive swellings. Scale bar : 10 µm. Scale bar ( blow up ): 2 µm
Article Snippet: For visualization of F-actin Alexa Flour 532 conjugated Phalloidin (Invitrogen) was used.
Techniques: In Vitro, Transduction, Cell Culture, Staining, Microscopy, Two Tailed Test