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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Dynactin1 depletion leads to neuromuscular synapse instability and functional abnormalities

Fig. 2

CaP growth defect is independent of cytoskeleton dynamics modulation. a Actin filopodia dynamics is assayed by time-lapse imaging of single CaP cell arbors expressing membrane-bound reporter lyn-GFP, from 2dpf to 4dpf. Example of confocal z-stack projection of a 2dpf CaP, with an overlay showing total unstable filopodia in red. b Quantification of filopodia dynamics over 10 min reveals no change in total unstable filopodia length, number or average length for 1dpf, 2dpf, 3dpf or 4dpf cells, with the exception of total unstable filopodia length at 2dpf, which was found to be slightly diminished. c Microtubule growth was determined by time-lapse imaging of eb3-GFP comets at both 2dpf and 6dpf. d Quantification of extracted kymograms shows no change in microtubule growth at either timepoint, as determined by average distance, duration and average speed of comet runs. e Microtubule capture at putative synapses was assayed by expression of a synaptic marker (rab3-tagRFP, in red) simultaneously with eb3-GFP (in green) at 2dpf and 6dpf. f Quantification of microtubule capture at putative synapses, density of terminating eb3 comets or putative synapses per axonal segment reveal this process was not affected by loss of Dynactin1a. Data presented as average +/− SEM. (b: 1dpf n = 10,5; 2dpf n = 8,10, 3dpf n = 8,8, 4dpf n = 6,10; d: 2dpf n = 24, 22, 6dpf n = 22,20; f: 2dpf n = 15, 28, 6dpf n = 8,12)

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