Fig. 12

Model of npr-1 dependent effects on pathogen defense in the N2 C. elegans strain. Exposure to both pathogens leads to an npr-1 dependent activation of carbohydrate-binding factors, such as C-type lectin-like proteins, and also two central immune signaling cascades, the p38 MAPK and the insulin-like pathways, which could all enhance pathogen resistance (middle part of the graph). Upon exposure to P. aeruginosa PA14 (right side), npr-1 also influences the activation of a general stress response, via one or several GATA transcription factors(s), which increases oxidative stress resistance and thus resistance to the pathogen. The response to B. thuringiensis (left side) is mediated by npr-1 through one or several Ebox transcription factors, resulting in a reduced oxidative stress response and increased metabolic activity as a possible cause of enhanced pathogen susceptibility. Arrows with light colors indicate uncertain connections