Fig. 10.

Cell autonomous and non-autonomous mechanisms influence nlp-29 expression. Quantitative RT-PCR analysis of nlp-29 gene expression level showing the infection-associated “fold induction” (infected/non-infected values) in worms treated with positive and negative RNAi control clones (targeting dcar-1 and sta-1, respectively) or clones that provoke a UPR^mt (targeting ant-1.1, atp-4, spg-7, ucr-1, and gas-1) in a wild-type (a) or the intestine-specific RNAi strain MGH171 (b) for 30 h before infection with D. coniospora for 18 h. Results are the average (± SD) from four and three experiments, respectively (see Additional file 11: Table S10). The difference between control and gas-1(RNAi) is not significant (ns) in either strain; * P < 0.05 (unpaired t-test). The SD for dcar-1 in (b) is 14. c Simplified model of pathways and processes involved in the regulation of nlp-29. The screen identified Hipi genes that modulate the adhesion of spores to the worm cuticle, and Nipi genes (central box) required for the expression of nlp-29 upon osmotic stress and infection (purple), or only after infection (yellow), acting downstream (below horizontal line) or upstream of or parallel to GPA-12. Only a very limited number of genes are shown; those in bold were identified in the screen. The Nipi genes fall into multiple functional categories; some are listed on the left, positioned arbitrarily; pointed and flat arrows indicate positive and negative regulation, respectively