Activation of the Caenorhabditis elegans FOXO family transcription factor DAF-16 by pathogenic Bacillus thuringiensis.

The FOXO family of transcription factors have recently been implicated in innate immunity, especially in case of DAF-16 from the nematode Caenorhabditis elegans. However, previous studies with this nematode proposed that DAF-16 is not directly activated by pathogens. Rather, DAF-16 mediates resistance if activated by some other cue as part of a general stress response. We specifically tested this notion by analysis of DAF-16 nuclear translocation and thus regulatory activity upon exposure to pathogenic Bacillus thuringiensis. Our results demonstrate that DAF-16 nuclear translocation is indeed particularly induced in response to bacterial pathogenicity, whereas infection load alone has little effect. Translocation is strongest at an early time point, suggesting a role during the immediate immune response. The increased DAF-16 availability is associated with higher resistance and a reduction in feeding behaviour. Taken together, our data highlight that a FOXO transcription factor directly responds to pathogens and thus contributes to immune defence.