NHR-14 loss of function couples intestinal iron uptake with innate immunity in through PQM-1 signaling.

Iron is essential for survival of most organisms. All organisms have thus developed mechanisms to sense, acquire and sequester iron. In s, iron uptake and sequestration are regulated by HIF-1. We previously showed that mutants are developmentally delayed when grown under iron limitation. Here we identify , encoding a nuclear receptor, in a screen conducted for mutations that rescue the developmental delay of mutants under iron limitation. loss upregulates the intestinal metal transporter SMF-3 to increase iron uptake in mutants. mutants display increased expression of innate immune genes and DAF-16/FoxO-Class II genes, and enhanced resistance to . These responses are dependent on the transcription factor PQM-1, which localizes to intestinal cell nuclei in mutants. Our data reveal how utilizes nuclear receptors to regulate innate immunity and iron availability, and show iron sequestration as a component of the innate immune response.