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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: A proteomic analysis of LRRK2 binding partners reveals interactions with multiple signaling components of the WNT/PCP pathway

Fig. 5

LRRK2 inhibits the activity of WNT/β-catenin pathway – an indirect read-out of WNT/PCP signaling activity. a Scheme of the Lrrk2 truncated vectors. b TOPFlash assay in HEK293T cells overexpressing LRRK2-WT or truncations. LRRK2 suppresses the basal activity of WNT/β-catenin signaling. This effect is lost with the most severe LRRK2 truncations, LRRK2-KINASE, WD40 and LRRS, that lack RocCOR domain. c LRRK2 together with PRICKLE1 increases the TOPFlash activity. This effect is lost in mutants that lacked the LRRs domain and the Ankyrin repeats, but is partially maintained in the mutant missing only the Armadillo domain (dHEAT). d LRRK2 PD mutants did not significantly inhibit TOPFlash (Mann Whitney t test). e DVL2 alone and together with LRRK2 strongly activates WNT/β-catenin signaling. PRICKLE1 down regulates the DVL2-dependent activation even in presence of LRRK2. ANOVA with Holm-Sidak multi-comparison test and Mann Whitney T-test (for the PD mutants) was used for statistical analysis. Data show mean (N>3) and standard deviation

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