Detailed Information on Publication Record
2018
Adipokinetic hormone and adenosine interfere with nematobacterial infection and locomotion in Drosophila melanogaster
IBRAHIM, Emad, Pavel DOBEŠ, Martin KUNC, Pavel HYRŠL, Dalibor KODRÍK et. al.Basic information
Original name
Adipokinetic hormone and adenosine interfere with nematobacterial infection and locomotion in Drosophila melanogaster
Name in Czech
Adipokinetic hormone and adenosine interfere with nematobacterial infection and locomotion in Drosophila melanogaster
Authors
IBRAHIM, Emad (818 Egypt), Pavel DOBEŠ (203 Czech Republic, belonging to the institution), Martin KUNC (203 Czech Republic, belonging to the institution), Pavel HYRŠL (203 Czech Republic, guarantor, belonging to the institution) and Dalibor KODRÍK (203 Czech Republic)
Edition
Journal of Insect Physiology, Kidlington, England, Elsevier, 2018, 0022-1910
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30105 Physiology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 2.862
RIV identification code
RIV/00216224:14310/18:00100913
Organization unit
Faculty of Science
UT WoS
000434751100021
Keywords (in Czech)
Adipokinetický hormon; adenosin; Drosophila; hlístice; oxidativní stres; lokomoce
Keywords in English
Adipokinetic hormone; adenosine; Drosophila; nematode; oxidative stress; locomotion
Tags
International impact, Reviewed
Změněno: 23/4/2024 11:15, Mgr. Michal Petr
V originále
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.
In Czech
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.
Links
| GA17-03253S, research and development project |
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