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. 2020 Jul 20;223(14):jeb221622. doi: 10.1242/jeb.221622

Fig. 6.

Fig. 6.

AP-1 and lola-PT mediate p38Kb transcription and oxidative stress resistance. (A,B) Levels of p38Kb transcription in response to over-expression of AP-1 under control conditions (A) and with exposure to 20 mmol l−1 paraquat (B). (C,D) Levels of p38Kb transcription in response to over-expression of lola-PT under control conditions (C) and with exposure to 20 mmol l−1 paraquat (D). Findings (means±s.e.m.) for A–D are based on 3 biological replicates for each genotype; each replicate consists of 6 individual flies. Significance was determined by one-tailed Student's t and Wilcoxon signed-rank tests. (E–H) Resistance to 20 mmol l−1 paraquat (E,F) or 10 mmol l−1 paraquat (G,H) of AP-1 (E,G) or lola-PT (F,H) over-expressing flies (red). Controls are outcrossed GAL4 (black) and transgene (gray) flies. In E and F the number of animals and replicates per genotype was as follows: MHC:AP-1 n=120, 8 replicates; w1118:AP-1 n=145, 10 replicates; MHC:lola-PT n=123, 8 replicates; w1118:lola-PT n=106, 7 replicates; and MHC:w1118 n=75, 5 replicates. In G and H, the number of animals and replicates per genotype was as follows: MHC:AP-1 n=90, 9 replicates; w1118:AP-1 n=66, 7 replicates; MHC:lola-PT n=98, 10 replicates; w1118:lola-PT n=68, 7 replicates; and MHC:w1118 n=75, 5 replicates. Differences in survival were assayed using the log-rank test.