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Inhibition of the oligosaccharyl transferase in Caenorhabditis elegans that compromises ER proteostasis suppresses p38-dependent protection against pathogenic bacteria

Fig 5

OST complex increases the expression of several PMK-1-regulated genes under PA14-infected conditions.

(A) RNAi targeting each OST component (ZK686.3, ribo-1, stt-3, ostb-1, or ostd-1) reduced the induction of T24B8.5p::GFP by PA14 infection. pmk-1 RNAi was used as a positive control. Scale bar indicates 500 μm. Different from the genetic inhibition of the OST complex, treatment with tunicamycin (5 μg/ml) did not alter the level of T24B8.5p::GFP with or without PA14 infection (S5C Fig). (B) Quantification of data in panel A (n ≥ 20 from three independent experiments). (C-E) qRT-PCR analysis data showing the mRNA levels of three selected PMK-1-regulated genes, T24B8.5 (C), C17H12.8 (D), and K08D8.5 (E), upon knocking down indicated OST components with or without PA14 infection (n ≥ 3). pmk-1 RNAi was used as a positive control. (F-G) qRT-PCR analysis data showing the mRNA levels of two selected ZIP-2-regulated genes, irg-1 (F) and irg-2 (G), upon knocking down indicated OST components with or without PA14 infection (n = 4). Error bars indicate SEM. p values were calculated by using two-tailed Student’s t-test (*p < 0.05, **p < 0.01, ***p < 0.001).

Fig 5

doi: https://doi.org/10.1371/journal.pgen.1008617.g005