strains used in this study were n2 bristol wt strain , sj4005 phsp-4gfp(zcis4 ) , zd305 pmk-1(km25);phsp-4gfp(zcis4 ) , zd441 atf-7(qd22 qd130 ) ; phsp-4gfp(zcis4 ) , zd361 xbp-1(zc12 ) , rb545 pek-1(ok275 ) , rb772 atf-6(ok551 ) , zd363 xbp-1(zc12);pmk-1(km25 ) , zd416 xbp-1(tm2457 ) , zd417 xbp-1(tm2457);pmk-1(km25 ) , zd418 xbp-1(tm2482 ) and zd419 xbp-1(tm2482);pmk-1(km25 ) . all p. aeruginosa ( strain pa14 ) plates were prepared as described13 , exceptions are detailed in supplementary methods . for tunicamycin treatments , tunicamycin was added to e. coli plates at 5 g / ml final concentration . images were acquired with an axioimager z1 microscope using worms anesthetized in 0.1% sodium azide . l1 larvae were synchronized by hypochlorite treatment , washed onto op50 plates and grown at 20 c for 23 h on op50 , then washed in m9 onto treatment plates . rna and qrt - pcr methods are detailed in supplementary methods . for development assays , strains were egg laid in parallel onto 4 plates each of pa14 and op50 ( at least 80 eggs for each strain and treatment ) , and fraction of worms growing to at least the l4 larval stage (  l4 +  ) between the plates was averaged . rnai by feeding of bacteria30 was performed as described by propagating stains on e. coli ht115 carrying the rnai clones as indicated at 20 c , and adult progeny were used to lay eggs in experiments , which were performed at 25 c. details regarding rnai clones are in supplementary methods .
the detection and compensatory response to the accumulation of unfolded proteins in the endoplasmic reticulum ( er ) , termed the unfolded protein response ( upr ) , represents a conserved cellular homeostatic mechanism with important roles in normal development and in the pathogenesis of disease1 . 
 the ire1-xbp1/hac1p pathway is a major branch of the upr that has been conserved from yeast to human2,3,4,5,6 . 
 xbp-1 is required for the differentiation of the highly secretory plasma cells of the mammalian adaptive immune system7,8 , but recent work also points to reciprocal interactions between the upr and other aspects of immunity and inflammation9,10,11 . 
 we have been studying innate immunity in the nematode caenorhabditis elegans , having established a key role for a conserved pmk-1 p38 mitogen - activated protein kinase ( mapk ) pathway in mediating resistance to microbial pathogens12 . here 
 , we show that during c. elegans development , xbp-1 has an essential role in protecting the host during activation of innate immunity . 
 activation of the pmk-1-mediated response to infection with pseudomonas aeruginosa induces the xbp-1-dependent upr . whereas a loss - of - function xbp-1 mutant develops normally in the presence of relatively non - pathogenic bacteria , infection of the xbp-1 mutant with p. aeruginosa leads to disruption of er morphology and larval lethality . 
 unexpectedly , the larval lethality phenotype on pathogenic p. aeruginosa is suppressed by loss of pmk-1-mediated immunity . 
 furthermore , hyperactivation of pmk-1 causes larval lethality in the xbp-1 mutant even in the absence of pathogenic bacteria . 
 our data establish innate immunity as a physiologically relevant inducer of er stress during c. elegans development and suggest that an ancient , conserved role for xbp-1 may be to protect the host organism from the detrimental effects of mounting an innate immune response to microbes .