Fig. 8: Blocking autophagy protects ALM neurons against oxidative stress.
From: OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress
a Schematic representation of autophagosome biogenesis with molecules that act in the initiation and elongation stages. Autophagosomes then fuse with lysosomes to form autolysosomes, a process that is inhibited by chloroquine. b Quantification of the ALM cell death phenotype in wt and animals expressing two unc-51 alleles (e369 and e1189). c Quantification of the ALM cell death phenotype in non-transgenic (-) and transgenic (+) animals expressing UNC-51 under its endogenous promoter (punc-51::UNC-51) in either unc-51(e369) or wt background. d Quantification of the ALM cell death phenotype in non-transgenic animals (-) and transgenic siblings (+) expressing UNC-51 specifically in the mechanosensory neurons (pmec-7::UNC-51) in either unc-51(e369) or wt background. In panels (b–d), comparisons between groups were done using one-way ANOVA with a Tukey’s test for multiple comparisons. e Quantification of the ALM cell death phenotype in wt and atg-13(bp414) animals. f Quantification of the ALM cell death phenotype in wt and atg-3(bp412) animals. g Quantification of the ALM cell death phenotype in animals illuminated on control plates (H2O) versus plates containing 10 mM chloroquine (CQ). In panels (e–g) comparisons between groups were done using a two-tailed unpaired t-test. In panels b to g, bars represent mean values; N values are indicated in the graphs; error bars represent the SE of proportion, KillerRed was activated using microscope illumination.
