The C. elegans CCAAT-Enhancer-Binding Protein Gamma Is Required for Surveillance Immunity

• CEBP-2, the C. elegans ortholog of mammalian C/EBP-γ, promotes resistance to infection
• CEBP-2, like the ZIP-2 transcription factor, defends against translational block
• CEBP-2 mediates a response to perturbation in histone and mitochondrial function
• CEBP-2 and ZIP-2 are potential heterodimeric partners in surveillance immunity

SummaryPathogens attack host cells by deploying toxins that perturb core host processes. Recent findings from the nematode C. elegans and other metazoans indicate that surveillance or “effector-triggered” pathways monitor functioning of these core processes and mount protective responses when they are perturbed. Despite a growing number of examples of surveillance immunity, the signaling components remain poorly defined. Here, we show that CEBP-2, the C. elegans ortholog of mammalian CCAAT-enhancer-binding protein gamma, is a key player in surveillance immunity. We show that CEBP-2 acts together with the bZIP transcription factor ZIP-2 in the protective response to translational block by P. aeruginosa Exotoxin A as well as perturbations of other processes. CEBP-2 serves to limit pathogen burden, promote survival upon P. aeruginosa infection, and also promote survival upon Exotoxin A exposure. These findings may have broad implications for the mechanisms by which animals sense pathogenic attack and mount protective responses.

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