| 181650 |
G5EED4 |
NIPI3_CAEEL |
Protein nipi-3 (No induction of peptide after drechmeria infection protein 3) (Tribbles homolog nipi-3) |
DISRUPTION PHENOTYPE |
Arrested development at the second to third larval stages (L2-L3) and lethality between 5-10 days after hatching (PubMed:27927209). Small and dumpy body morphology at the second to third larval stages (L2-L3), abnormal pharyngeal morphology, sterility (PubMed:27927209). Growth and fertility defects are suppressed in a cebp-1 mutant background (PubMed:27927209). Lethality is suppressed in several mutant backgrounds, including tir-1, or kinases nsy-1, sek-1 or mak-2 (PubMed:27927209). Levels of phosphorylated, active p38/MAPK pmk-1 are significantly increased (PubMed:27927209). Increased levels of cebp-1 mRNA in multiple tissues (PubMed:27927209). RNAi-mediated knockdown results in a loss of nlp-29 expression upon fungal infection (PubMed:18394898). No other obvious phenotype (PubMed:18394898). Knockdown results in a drastic reduction in transcription of gst-4 and gcs-1 mRNAs during infection by P.aeruginosa or P.faecalis, or treatment with the oxidant, arsenite (PubMed:34407394). RNAi-mediated knockdown targeted to intestinal cells causes hypersusceptibility to Gram-negative bacterium P.aeruginosa or to Gram-positive bacterium E.faecalis and also to the P.aeruginosa toxin ToxA (PubMed:27927200, PubMed:34407394). Simultaneous knockdown with vhp-1, targeted to intestinal cells, results in partial rescue of the nipi-3 pathogen sensitivity phenotype (PubMed:34407394). {ECO:0000269|PubMed:18394898, ECO:0000269|PubMed:27927200, ECO:0000269|PubMed:27927209, ECO:0000269|PubMed:34407394}. |