Potential Nematode Alarm Pheromone Induces Acute Avoidance in Caenorhabditis elegans

It is crucial for animal survival to detect dangers such as predators. A good indicator of dangers is injury of conspecifics. Here we show that fluids released from injured conspecifics invoke acute avoidance in both free-living and parasitic nematodes. Caenorhabditis elegans avoids extracts from closely related nematode species but not fruit fly larvae. The worm extracts have no impact on animal lifespan, suggesting that the worm extract may function as an alarm instead of inflicting physical harm. Avoidance of the worm extract requires the function of a cGMP signaling pathway that includes the cGMP-gated channel TAX-2/TAX-4 in the amphid sensory neurons ASI and ASK. Genetic evidence indicates that the avoidance behavior is modulated by the neurotransmitters GABA and serotonin, two common targets of anxiolytic drugs. Together, these data support a model that nematodes use a nematode-specific alarm pheromone to detect conspecific injury

High-content behavioral profiling reveals neuronal genetic network modulating Drosophila larval locomotor program

Abstract Background Two key questions in understanding the genetic control of behaviors are: what genes are involved and how these genes interact. To answer these questions at a systems level, we conducted high-content profiling of Drosophila larval locomotor behaviors for over 100 genotypes. Results We studied 69 genes whose C. elegans orthologs were neuronal signalling genes with significant locomotor phenotypes, and conducted RNAi with ubiquitous, pan-neuronal, or motor-neuronal Gal4 drivers. Inactivation of 42 genes, including the nicotinic acetylcholine receptors nAChRα1 and nAChRα3, in the neurons caused significant movement defects. Bioinformatic analysis suggested 81 interactions among these genes based on phenotypic pattern similarities. Comparing the worm and fly data sets, we found that these genes were highly conserved in having neuronal expressions and locomotor phenotypes. However, the genetic interactions were not conserved for ubiquitous profiles, and may be mildly conserved for the neuronal profiles. Unexpectedly, our data also revealed a possible motor-neuronal control of body size, because inactivation of Rdl and Gαo in the motor neurons reduced the larval body size. Overall, these data established a framework for further exploring the genetic control of Drosophila larval locomotion. Conclusions High content, quantitative phenotyping of larval locomotor behaviours provides a framework for system-level understanding of the gene networks underlying such behaviours

Additional file 1: Table S1. of High-content behavioral profiling reveals neuronal genetic network modulating Drosophila larval locomotor program

Genes studied. List of the gene names, FlyBase IDs of the genes, the Bloomington stock numbers of fly strains used, and the worm orthologs of the fly genes (XLSX 12 kb)

Additional file 2: Table S2. of High-content behavioral profiling reveals neuronal genetic network modulating Drosophila larval locomotor program

Locomotive profiles of genes with significant phenotypes. Profiles are composed of normalized values for ten locomotive parameters. Profiles for both neuronal and ubiquitous RNAi are listed. The summary page lists genes with significant phenotypes (XLSX 26 kb)

Additional file 3: Table S3. of High-content behavioral profiling reveals neuronal genetic network modulating Drosophila larval locomotor program

Genetic interactions inferred from locomotive profiles. Predicted genetic interactions with |PCC| > 0.7 and GeneOrienteer score over 4 (XLSX 12 kb)

Potential nematode alarm pheromone induces acute avoidance in C. elegans: Source code, executable files, and sample images.

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