Abstract
As infectious diseases pose a threat to host integrity, eukaryotes have evolved mechanisms to eliminate pathogens. In addition to develop strategies reducing infection, animals can engage in behaviours that lower the impact of the infection. The molecular mechanisms by which microbes impact host behaviour are not well understood. We demonstrate that bacterial infection of Drosophila females reduces oviposition and that peptidoglycan, the component that activates Drosophila antibacterial response, is also the elicitor of this behavioral change. We show that peptidoglycan regulates egg laying rate by activating NF-B signaling pathway in octopaminergic neurons and that, a dedicated peptidoglycan degrading enzyme acts in these neurons to buffer this behavioural response. This study shows that a unique ligand and signaling cascade are used in immune cells to mount an immune response and in neurons to control fly behavior following infection. This may represent a case of behavioural immunity.
Article and author information
Author details
Funding
Centre National de la Recherche Scientifique (24567)
- Julien Royet
Equipe Fondation pour la Recherche Médicale (DEQ20140329541)
- Julien Royet
Investissements d'avenir-Labex INFORM (ANR-11-LABx-0054)
- Julien Royet
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Mani Ramaswami, Trinity College Dublin, Ireland
Publication history
- Received: September 29, 2016
- Accepted: February 26, 2017
- Accepted Manuscript published: March 7, 2017 (version 1)
- Version of Record published: March 24, 2017 (version 2)
Copyright
This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
Metrics
-
- 2,961
- Page views
-
- 640
- Downloads
-
- 25
- Citations
Article citation count generated by polling the highest count across the following sources: Scopus, Crossref, PubMed Central.