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. 2009 Sep 18;5(9):e1000657. doi: 10.1371/journal.pgen.1000657

Figure 6. Derepression of CEP-1 transcriptional activity by nol-6 RNAi activates immunity against S. enterica.

Figure 6

(A) Quantitative RT-PCR analysis of 7 cep-1–dependent genes in nematodes grown on dsRNA for vector control or dsRNA for nol-6. Data were analyzed by normalization to pan-actin (act-1,-3,-4) and relative quantification using the comparative-cycle threshold method. Student's exact t test indicates that differences among the groups are significantly different; bar graphs correspond to mean±SEM (n = 3). (B) Wild type and sym-1(mn601) nematodes grown on dsRNA for vector control or dsRNA for nol-6 were fed S. enterica, and the number of live versus dead animals was scored over time. Vector vs. sym-1(mn601): p = 0.0002. For each condition, 60 animals were used. This experiment was performed in duplicate. (C) Wild type and sym-1(mn601) nematodes were fed S. enterica/GFP or S. enterica/GFP for 48 hours, and the percentages of worms exhibiting pharyngeal invasion of S. enterica were quantified. Wild type vs. sym-1(mn601) S. enterica/GFP: p<0.0001. For each condition, approximately 100 animals were used. (D) Mechanism by which disruption of the nucleolus may lead to enhanced resistance to pathogen through the activation of CEP-1. Inhibition of nol-6 and other nucleolar proteins via RNAi or mutation disrupts nucleolar integrity leading to an upregulation of CEP-1-dependent transcription and an increase in resistance to both S. enterica and P. aeruginosa. Disruption of the nucleolus may also lead to enhanced resistance to P. aeruginosa through the activity of PMK-1 and DAF-16.