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. 2022 Nov 23;22(3):e13741. doi: 10.1111/acel.13741

FIGURE 4.

FIGURE 4

Neuronal HLH‐30/TFEB mediates thermoresistance through peripheral mitochondrial fragmentation. (a and b) Survival analyses of wildtype animals fed control RNAi (L4440, solid lines) or RNAi against (a) drp‐1 and (b) eat‐3 (dotted lines) at 37°C heat stress. Animals developed at 20°C to the L4 larval stage on OP50 were transferred onto bacteria expressing RNAi for 48 h and exposed to 37°C heat stress until death. Data are representatives of 2 independent replicates (n = 89–180/RNAi) and comparisons were made by Mantel‐Cox log‐rank (*, p < 0.05; in comparison to control RNAi). (c) Representative images of muscle mitochondrial morphology with the body wall muscle mitochondrial reporter (Mito::GFP) and of muscle morphology with the body wall muscle myosin reporter (MYO‐3::GFP) in wildtype, hlh‐30(tm1978), and neuronal HLH‐30/TFEB rescued animals at 20°C (arrow, GFP in muscle nuclei) or after 37°C heat stress for 3 h. Scale bars = 20 μM. (d) Analysis of mitochondrial connectivity in wildtype, hlh‐30(tm1978), and neuronal HLH‐30/TFEB rescued animals after 37°C heat stress for 3 h. (c, d) Animals were developed at 20°C to day 1 of adulthood and exposed to 37°C heat stress for 3 h. Data are representatives of 4 independent replicates (per strain; n = 40, number of ROIs = 117–150) and comparisons were made by Kruskal–Wallis for each mitochondrial feature (presented as mean ± SD; n.s, p ≥ 0.05; ***, p < 0.001; ****, p < 0.0001).