Fig. 2

MLKL deficiency improves motor capability in homozygous A53T synuclein transgenic (Tg) mice. Wild-type (WT, n = 10), Tg-Mlkl^+/+ (n = 7), and Tg-Mlkl^−/− mice (n = 13) around 10–12 months old were examined for different motor activities as described in the Methods section. a. Schematic of the crossbreeding between A53T transgenic mice (expressing mutant human α-synuclein) and MLKL KO mice. b-c. Immunoblotting analysis of the protein expression levels of α-synuclein (α-Syn) and MLKL in multiple tissues from the Tg-Mlkl^+/+ and Tg-Mlkl^−/− mice. d-f. The autonomous trajectory map of WT, Tg-Mlkl^+/+, and Tg-Mlkl^−/− mice in the open field test. Tg-Mlkl^−/− mice exhibited more entries (e) and times (f) in the center region than Tg-Mlkl^−/− mice. g. The average time required for the WT, Tg-Mlkl^+/+, and Tg-Mlkl^−/− mice to descend the pole. h. WT, Tg-Mlkl^+/+, and Tg-Mlkl^−/− mice were scored for latency to fall on the accelerating rotarod. i-l. Performance of mice in the elevated plus-maze test (EPMT). i. The autonomous trajectory maps of WT, Tg-Mlkl^+/+, and Tg-Mlkl^−/− mice in the EPMT were recorded. j. The total distance traveled in 5 min was shown. The Tg-Mlkl^−/− mice had more entries into the open arms (k) and spent more time in the anxiety-provoking open arms (l) than the Tg-Mlkl^−/−mice. m. Detection of depression with the tail suspension test. The Tg-Mlkl^−/− mice showed a significant reduction in the duration of immobility compared with the control mice. n. Long-term pole test results from 2–18 months, comparing WT, Tg-Mlkl^+/+, and Tg-Mlkl^−/− mice. o. Survival curves for Tg-Mlkl^+/+ (n = 19) and Tg-Mlkl^−/− (n = 37) mice. All data are representative of three independent experiments. The error bars represented the standard deviations (SD). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns, no significance