Research Paper Volume 12, Issue 9 pp 8202—8220

A cellular surveillance and defense system that delays aging phenotypes in C. elegans

Figure 4. Aging and Pathogen Infection activate ZIP-2 through a distinct mechanism. (A) (I) irg-1p::GFP expression patterns of wild-type (N2) and zip-2(ok3730) mutant worms at day 1 or day 8 of adulthood. Each strain was transferred to dead bacterial plates at day 1 of adulthood. Scale bar: 100 μm. (II and III) Relative GFP intensity in intestine. D1 and D8 represent day 1 and day 8, respectively. GFP intensity of individual worms was normalized to the minimum GFP intensity value among all GFP intensity values. Two independent experimental data. (B) (I) Representative images of mitochondrial morphologies in body wall muscle at day 11 of adulthood in wild-type (n=49) and zip-2(ok3730) mutant worms (n=36). Scale bar: 50 μm. (II) Qualitative analysis of mitochondrial morphology observed at day 11 of adulthood in wild-type and zip-2(ok3730) mutant worms. Bars represent the proportion of worms with fragmented mitochondrial form. The n value represents total number of tested worms by two independent experiments. (C, D) Relative irg-1p::GFP (C) or zip-2p::GFP (D) intensity in atfs-1(gk3094) mutant worms at day 1 or day 8 of adulthood. Two independent experimental data. (E) irg-1p::GFP expression pattern at day 1 of adulthood of atfs-1(gk3094) in DMSO or Rotenone or TTFA assay plates. Scale bar: 100 μm. (F) A schematic diagram of ZIP-2 activation in aging or by pathogen infection and its biological functions in C. elegans. Shapiro-Wilk normality test was used to assess normal distribution of the samples. Significance was determined using a two-tailed, unpaired t-test. ** P < 0.01, *** P < 0.001, **** P < 0.0001.