Adipokinetic hormone and adenosine interfere with nematobacterial infection and locomotion in Drosophila melanogaster
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
29627353
DOI
10.1016/j.jinsphys.2018.04.002
PII: S0022-1910(18)30078-7
Knihovny.cz E-resources
- Keywords
- Adenosine, Adipokinetic hormone, Drosophila, Locomotion, Nematode, Oxidative stress,
- MeSH
- Adenosine metabolism MeSH
- Antibiosis * MeSH
- Drosophila melanogaster growth & development microbiology parasitology physiology MeSH
- Bacterial Physiological Phenomena MeSH
- Insect Hormones metabolism MeSH
- Pyrrolidonecarboxylic Acid analogs & derivatives metabolism MeSH
- Larva growth & development microbiology parasitology physiology MeSH
- Oligopeptides metabolism MeSH
- Rhabditida physiology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adenosine MeSH
- adipokinetic hormone MeSH Browser
- Insect Hormones MeSH
- Pyrrolidonecarboxylic Acid MeSH
- Oligopeptides MeSH
This study examined how adipokinetic hormone (AKH) and adenosine affect defense responses in Drosophila melanogaster larvae infected with entomopathogenic nematodes (EPN, Steinernema carpocapsae and Heterorhabditis bacteriophora). Three loss-of-function mutant larvae were tested: Akh1, AdoR1 (adenosine receptor), and Akh1 AdoR1. Mortality decreased in all mutants post-EPN infection compared with the control (w1118). Additionally, co-application of external AKH with EPN significantly increased mortality beyond rates observed in EPN-only treatment, while also elevating carbon dioxide production, a measure of metabolism. Furthermore trehalose levels increased in both w1118 and Akh1 larvae post-EPN infection, but the latter group exhibited a lower increase and total trehalose levels. Interestingly, baseline trehalose was relatively high in untreated AdoR1 and Akh1 AdoR1 mutants, with levels remaining unaffected by infection. Infection also elevated haemolymph lipid content overall, but the different mutations did not substantially influence this change. In contrast, haemolymph protein content dropped after EPN infection in all tested groups, but this decline was more intense among Akh1. In uninfected larvae mutations decreased antioxidative capacity in Akh1 and increased in AdoR1, however, its post-infection increases were similar in all mutants, suggesting that antioxidant response in Drosophila involves mechanisms also beyond AKH and adenosine. Furthermore, AKH application in w1118 larvae significantly increased movement distance and percentage of larval activity, but reduced velocity. Mutations of Akh and AdoR did not strongly affect locomotion.
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