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. 2012 May 11;109(22):8582–8587. doi: 10.1073/pnas.1120510109

Fig. 2.

Fig. 2.

(A) KLC1 motor subunit composition of APP vesicles in KLC1 genotypes. KLC1+/+: nVesicles = 1,676, nAnimals = 4, nAxons = 20; KLC1+/−: nVesicles = 1,760, nAnimals = 4, nAxons = 19; KLC1−/−: nVesicles = 1,569, nAnimals = 3, nAxons = 17. BKGD denotes nonspecific colocalization of background staining between immunofluorescence channels outside of axonal projections. Error bars show SEM. (B) APP vesicle-associated anti-KLC1 intensity distributions in KLC1 genotypes. Distributions are presented as a function of relative frequency of the total number of APP vesicles detected, and to simplify comparison, plotted as line graphs using an intensity bin size of 20 AU. KLC1+/+: nVesicles = 895, nAnimals = 2, nAxons = 10; KLC1+/−: nVesicles = 1,041, nAnimals = 2, nAxons = 10; KLC1−/−: nVesicles = 1,126, nAnimals = 2, nAxons = 10. Error bars show SEM. (C) KLC1-mCherry (seed channel) vs. associated anti-KLC1 intensity correlation in WT axons. nAxons = 3, nKLC1-mCherry = 271. (D) Anti-APP intensity distributions in APP genotypes. WT: nAxons = 4; APP−/−: nAxons = 3. The upward intensity shift in anti-APP dynamic range is a result of increased exposure settings required to detect the low-level background APP signal in APP−/− cells. Bin size = 50 AU.