Fig. 3

The effect of human neuropeptide receptors on bordering and MeSa avoidance behavior of npr-1 null nematodes. a Assay layout for determining the bordering behavior of C. elegans nematodes. Adult hermaphrodites were transferred on a plate seeded with a defined bacterial lawn. Wild-type animals are dispersed randomly on the lawn (left) whereas npr-1 null mutant worms form aggregates at the border of the bacterial lawn (right). b Schematic depiction of the assay set-up determining MeSa avoidance. Assay plates lacking bacteria are divided into four quadrants, containing a drop of ethanol (EOH) and sodium azide, or MeSa and sodium azide, respectively. Nematodes are initially placed in the middle of a plate (left). In the time-course of the assay, they crawl to the quadrants with MeSa or EOH and get paralyzed by the sodium azide (right). EOH serves as control substance, as it does not have any effect on npr-1 mutant nematodes ([24] and Additional file 1: Figure S2). Worms in each quadrant are scored and MeSa avoidances is calculated. c The bordering phenotype of npr-1 mutant individuals can be slightly ameliorated by transgenic expression of npr-1 promoter-driven npr-1. Data are show as mean ± SD in at least four independent experiments (n ≥ 480). *p < 0.05; ***p < 0.001 compared to npr-1 mutants. d MeSa avoidance of npr-1 mutants is greatly reduced compared to wild-type animals. This phenotype is rescued by transgenic expression of npr-1 driven by a npr-1 promoter (npr-1; Ex [npr-1]). Data are shown as mean ± SD in at least six independent experiments (n ≥ 300). ***p < 0.001 compared to npr-1 mutants. e Reduced MeSa avoidance of npr-1 mutants is rescued by expression of several human neuropeptide receptors driven by a npr-1 promoter from a transgene (Ex [receptor]). Construct Ex [npr-1] (also shown in (d)) served as a positive control. Data are shown as mean ± SD in at least six independent experiments (n ≥ 300). *p < 0.05; ***p < 0.001 compared to npr-1 mutants