Fig. 2: HA-114 does not require classic stress and metabolic pathways in C. elegans for neuroprotection.

Neuroprotection provided by L. rhamnosus HA-114 was unaffected by a daf-16(mu86) deletion, nor by hsf-1(sy441) point mutation. Both sir-2.1 and aak-2 genes are not required for neuroprotection granted by HA-114 probiotics. b Aggregation was not altered by HA-114 in a polyQ model at L4 or at day 1 of adulthood. Scale bar = 100 μm. c HA-114 did not affect GFP expression of key genes of innate immune response (nlp-29), UPRmito response (hsp-6 and dve-1) or UPRER (hsp-4) Scale bar = 100 μm. For paralysis assays (a), curves were generated and compared using the log-rank (Mantel–Cox) test. TDP-43A315T;daf-16(mu86) on OP50 n = 248; TDP-43A315T;daf-16(mu86) on HA-114 n = 237; TDP-43A315T;hsf-1(sy441) on OP50 n = 279; TDP-43A315T;hsf-1(sy441) on HA-114 n = 237; TDP-43A315T;sir-2.1(ok434) on OP50 n = 118; TDP-43A315T;sir-2.1(ok434) on HA-114 n = 120; TDP-43A315T;aak-2(ok524) on OP50 n = 240; TDP-43A315T; aak-2(ok524) on HA-114 n = 239. For the aggregation assay (b), a two-way ANOVA was performed and for each conditions, n = 3 (with 237 worms evaluated over the 3 trials for OP50 L4, 236 worms for HA-114 L4, 230 worms for OP50 Day 1 adult and 216 worms for HA-114 Day 1 adult). For fluorescence quantification (c), an unpaired t test was performed and n are indicated in the figure. Data are presented as mean ± SEM. For boxplots, minimum, first quartile, median, third quartile, and maximum are shown.