The DAF-16/FOXO Transcription Factor Functions as a Regulator of Epidermal Innate Immunity

The caenorhabditis elegans daf-16 transcription factor is critical for diverse biological processes,particularly longevity and stress resistance. disruption of the daf-2 signaling cascade promotes daf-16 activation,and confers resistance to killing by pathogenic bacteria,such as pseudomonas aeruginosa,staphylococcus aureus,and enterococcus faecalis. however,daf-16 mutants exhibit similar sensitivity to these bacteria as wild-type animals,suggesting that daf-16 is not normally activated by these bacterial pathogens. in this report,we demonstrate that daf-16 can be directly activated by fungal infection and wounding in wild-type animals,which is independent of the daf-2 pathway. fungal infection and wounding initiate the gαq signaling cascade,leading to ca2+ release. ca2+ mediates the activation of bli-3,a dual-oxidase,resulting in the production of reactive oxygen species (ros). ros then activate daf-16 through a ste20-like kinase-1/cst-1. our results indicate that daf-16 in the epidermis is required for survival after fungal infection and wounding. thus,the egl-30-ca2+-bli-3-cst-1-daf-16 signaling represents a previously unknown pathway to regulate epidermal damage response. © 2013 zou et al.