The SCA-1/XBP-1 pathway in the intestine functions as a regulator of innate immunity mediated by PMK-1.

<p>(A) Both <i>xbp-1(zc12)</i> and <i>mir-233(n4761)</i> mutants were more sensitive than wild type (WT) worms to the killing by <i>P. aeruginosa</i> PA14. <i>P</i><0.01 versus WT. However, the mutation in <i>mir-233(n4761)</i> did not enhance susceptibility of the <i>xbp-1(zc12)</i> mutant to PA14 infection. (B) Although knockdown of <i>sca-1</i> by RNAi promoted the survival of worms to PA14 infection, the survival of <i>xbp-1(zc12)</i>; <i>sca-1</i> RNAi worms was comparable to that of the <i>xbp-1(zc12)</i> worms after PA14 infection. <i>P</i><0.01 versus WT+empty vector (EV). (C) The survival of the <i>pmk-1(km25)</i> mutant was partially restored by knockdown of <i>sca-1</i>. <i>P</i><0.001, <i>pmk-1(km25)</i> versus WT; <i>P</i><0.01, <i>pmk-1(km25)</i>; <i>sca-1</i> RNAi versus <i>pmk-1(km25)</i>+EV. (D) Intestinal-specific RNAi of <i>sca-1</i> enhanced resistance, whereas intestinal-specific RNAi of <i>xbp-1</i> led to enhanced sensitivity to PA14 infection. <i>P</i><0.01 versus control (EV). All the survival graphs represent combined results of three independent experiments.