Fig. 6From: CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s diseaseα-syn differentially accumulates in the nucleus of symptomatic zQ175 mice and colocalized with mtHTT. A, α-syn (4D6 antibody) IB in the striatum of WT, zQ175 and SNCAKO and B in WT, zQ175 and zQ175:CK2α’(±) mice at 12 months old. GAPDH used as loading control. C, α-syn protein levels analyzed by Image J from IB analyses (n = 5–6 mice/genotype). D, Nuclear/cytoplasmic fractionation of striatum samples from 12-month-old WT, zQ175 and SNCAKO mice. E, Quantification of nuclear α-syn from images in D (n = 4 mice/genotype, at least 3 images averaged/mouse). F, α-syn and HTT (EM48 antibody) IF images of dorsal striatum sections from 12 month old WT, zQ175 and zQ175:CK2α’(±) (n = 3 mice/genotype). White arrows indicate α-syn/HTT colocalization. Scale bar, 10 μm. G, Magnification of images from F. Scale bar, 2 μm. Grey circles represent nuclei. H Number of cytoplasmic and i nuclear EM48+ puncta (n = 3 mice/ genotype, 9 images averaged/mouse). J, Number of colocalized α-syn and EM48+ puncta calculated using Image J Puncta analysis plugin (n = 3 mice/genotype, 6–9 images averaged/mouse). Error bars denote mean ± SEM, values were analyzed by Student’s t-testBack to article page