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Expression cluster » WBPaper00064871:P.fluorescens_upregulated_AWA
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WBPaper00064871:P.fluorescens_upregulated_AWA
Algorithm:
P values are derived from two-sided exact test used in the R package edgeR and the FDR values are BenjaminiHochberg adjusted P values. FDR < 0.05 (set by WormBase Curator).Remarks:
Type: Bacteria InfectionAssociations
| Anatomy term | Definition |
|---|---|
| AWA | Neuron class of two ciliated neurons that are associated with the sheath cells of the amphid sensilla. |
| Life Stages | Definition |
|---|---|
| 1-day post-L4 adult hermaphrodite Ce | At 20 Centigrade: 24-48 hours after L4-adult molt. 4-5 days after first cleavage. |
References
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1
Pathogens generate ubiquitous selective pressures and host-pathogen interactions alter social behaviours in many animals<sup>1-4</sup>. However, very little is known about the neuronal mechanisms underlying pathogen-induced changes in social behaviour. Here we show that in adult Caenorhabditis elegans hermaphrodites, exposure to a bacterial pathogen (Pseudomonas aeruginosa) modulates sensory responses to pheromones by inducing the expression of the chemoreceptor STR-44 to promote mating. Under standard conditions, C. elegans hermaphrodites avoid a mixture of ascaroside pheromones to facilitate dispersal<sup>5-13</sup>. We find that exposure to the pathogenic Pseudomonas bacteria enables pheromone responses in AWA sensory neurons, which mediate attractive chemotaxis, to suppress the avoidance. Pathogen exposure induces str-44 expression in AWA neurons, a process regulated by a transcription factor zip-5 that also displays a pathogen-induced increase in expression in AWA. STR-44 acts as a pheromone receptor and its function in AWA neurons is required for pathogen-induced AWA pheromone response and suppression of pheromone avoidance. Furthermore, we show that C. elegans hermaphrodites, which reproduce mainly through self-fertilization, increase the rate of mating with males after pathogen exposure and that this increase requires str-44 in AWA neurons. Thus, our results uncover a causal mechanism for pathogen-induced social behaviour plasticity, which can promote genetic diversity and facilitate adaptation of the host animals.
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