Knockdown of adipokinetic hormone synthesis increases susceptibility to oxidative stress in Drosophila--a role for dFoxO?
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S.
PubMed
25814322
DOI
10.1016/j.cbpc.2015.03.006
PII: S1532-0456(15)00026-5
Knihovny.cz E-zdroje
- Klíčová slova
- Adipokinetic hormone, Drosophila, FoxO, Hydrogen peroxide, Oxidative stress,
- MeSH
- biologické markery metabolismus MeSH
- Drosophila melanogaster genetika fyziologie MeSH
- forkhead transkripční faktory genetika metabolismus MeSH
- geneticky modifikovaná zvířata MeSH
- hmyzí hormony antagonisté a inhibitory genetika metabolismus MeSH
- karbonylace proteinů účinky léků MeSH
- křížení genetické MeSH
- kyselina pyrrolidonkarboxylová analogy a deriváty antagonisté a inhibitory metabolismus MeSH
- léková rezistence MeSH
- MAP kinasový signální systém účinky léků MeSH
- messenger RNA metabolismus MeSH
- oligopeptidy antagonisté a inhibitory genetika metabolismus MeSH
- oxidační stres * MeSH
- oxidancia toxicita MeSH
- peroxid vodíku toxicita MeSH
- proteiny Drosophily antagonisté a inhibitory genetika metabolismus MeSH
- proteiny teplotního šoku genetika metabolismus MeSH
- regulace genové exprese * účinky léků MeSH
- rekombinantní proteiny chemie metabolismus MeSH
- RNA interference MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Názvy látek
- biologické markery MeSH
- DAKH peptide MeSH Prohlížeč
- forkhead transkripční faktory MeSH
- FOXO protein, Drosophila MeSH Prohlížeč
- hmyzí hormony MeSH
- kyselina pyrrolidonkarboxylová MeSH
- messenger RNA MeSH
- oligopeptidy MeSH
- oxidancia MeSH
- peroxid vodíku MeSH
- proteiny Drosophily MeSH
- proteiny teplotního šoku MeSH
- rekombinantní proteiny MeSH
Insect adipokinetic hormones (AKHs) are pleiotropic hormones known to play a protective role in response to oxidative stress (OS). However, the precise signaling pathways are unclear. We present evidence that AKH may primarily employ the Forkhead box class O transcription factor (FoxO) to exert this effect. The impact of knocking down AKH synthesis or its over-expression in its response to OS was studied in Drosophila melanogaster. AKH knockdown (AKH-RNAi) as well as AKH overexpression (AKH-oex) was achieved using the Gal-4/UAS system and controls were w(1118) (+/+), AKH-Gal4/+, UAS-AKH/+ and UAS-AKH-RNAi/+. Exposure to 80 μM hydrogen peroxide (HP) revealed that AKH-RNAi flies showed significantly higher mortality than AKH-oex or the respective control lines. This susceptibility was evidenced by significantly enhanced levels of protein carbonyls - a biomarker of OS, in AKH-RNAi flies compared to controls and AKH-oex flies. Interestingly, AKH-oex flies had the least amount of protein carbonyls. AKH-RNAi flies had significantly less dFoxO transcript and translated protein compared to control and AKH-oex flies in un-challenged condition as well as when challenged with HP. Sestrin - a major antioxidant defense protein and one of the targets of dFoxO - was also significantly down-regulated (both at mRNA and protein level) in AKH-RNAi flies (both unchallenged and challenged with HP) compared to control flies and flies with over-expressed AKH. These findings imply that dFoxO may act downstream of AKH as a transcription factor to mediate response to OS in D. melanogaster.
Citace poskytuje Crossref.org
Hormonal Regulation of Response to Oxidative Stress in Insects-An Update
