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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease

Fig. 4

Depletion of CK2α’ restored synaptic gene expression associated with α-syn-dependent regulation in zQ175 mice. A, Kruskal–Wallis test of module expressions between zQ175 (HD) mice and zQ175:CK2α’(±) mice. The y-axis is the negative log transformed p-values. B, Expressions of module “Greenyellow” in each mouse sample. C, IPA canonical pathway analysis, D, enrichment analysis of GO terms in CC (cellular component). E–F, Gene expression for microglia marker genes; A1-inducing and pan-reactive microglia genes (40) (E) and astrocyte markers representative of A1, A2 and pan-reactive astrocytes genes (40) (F) in WT, zQ175, CK2α’(±) and zQ175:CK2α’(±) mice. G, H, Mean log2 fold change between zQ175 and zQ175:CK2α’(±) mice compared to WT for genes representative of the HD-astrocyte molecular signature (41) (G), and the CK2α’-mediated RNA signature (H). Purple asterisk (*) indicates synaptic function, () indicates genes present in the Greenyellow module. i, IPA canonical pathway analysis for the CK2α’-mediated RNA signature. FDR < 0.1 was used for all gene expression analyses

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