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. 2019 Nov 12;19(1):e13065. doi: 10.1111/acel.13065

Figure 3.

Figure 3

Reduction in ER‐mitochondrial Ca2+ signaling in sel‐12 mutants rescues premature polyQ aggregation. (a) Quantification of Q35::YFP aggregation in day 3 adult wild‐type, sel‐12(ar131), and sel‐12(ty11) animals grown on RNAi plates seeded with either empty vector (EV) or itr‐1(RNAi) (N = 30 animals per group). (b) Quantification of Q35::YFP aggregation in wild‐type, sel‐12(ar131), sel‐12(ty11), crt‐1(jh101); sel‐12(ar131) and crt‐1(jh101); sel‐12(ty11) mutant animals at day 3 adulthood (N = 25 animals per group). (c) Quantification of Q35::YFP aggregation in wild‐type, sel‐12(ar131), sel‐12(ty11), mcu‐1(tm6026); sel‐12(ar131) and mcu‐1(tm6026); sel‐12(ty11) at day 3 adulthood (N = 25 animals per group). (d) Quantification of Q35::YFP aggregation in wild‐type, sel‐12(ar131) and sel‐12(ty11) animals grown in the absence or presence of 10 μg/ml tunicamycin at day 3 adulthood (N = 20 animals per group). Data are displayed as mean ± SEM, and all comparisons have been made to wild‐type animals or indicated strains. ns p > .05, **p < .01, and ***p < .001 were determined using one‐way ANOVA