Adenosine receptor ant its downstream targets, Mod(mdg4) and Hsp70, work as a signaling pathway modulating cytotoxic damage in Drosophila
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F21%3A00541060" target="_blank" >RIV/60077344:_____/21:00541060 - isvavai.cz</a>
Výsledek na webu
<a href="https://www.frontiersin.org/articles/10.3389/fcell.2021.651367/pdf" target="_blank" >https://www.frontiersin.org/articles/10.3389/fcell.2021.651367/pdf</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3389/fcell.2021.651367" target="_blank" >10.3389/fcell.2021.651367</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Adenosine receptor ant its downstream targets, Mod(mdg4) and Hsp70, work as a signaling pathway modulating cytotoxic damage in Drosophila
Popis výsledku v původním jazyce
Adenosine (Ado) is an important signaling molecule involved in stress responses. Studies in mammalian models have shown that Ado regulates signaling mechanisms involved in ‘danger-sensing’ and tissue-protection. Yet, little is known about the role of Ado signaling in Drosophila. In the present study, we observed lower extracellular Ado concentration and suppressed expression of Ado transporters in flies expressing mutant huntingtin protein (mHTT). We altered Ado signaling using genetic tools and found that the overexpression of Ado metabolic enzymes, as well as the suppression of Ado receptor (AdoR) and transporters (ENTs), were able to minimize mHTT-induced mortality. We also identified the downstream targets of the AdoR pathway, the modifier of mdg4 (Mod(mdg4)) and heat-shock protein 70 (Hsp70), which carry out its function. Finally, we showed that a decrease in Ado signaling affect other Drosophila stress reactions, including paraquat and heat-shock treatments. Our study provides important insights into how Ado regulates stress responses in Drosophila.
Název v anglickém jazyce
Adenosine receptor ant its downstream targets, Mod(mdg4) and Hsp70, work as a signaling pathway modulating cytotoxic damage in Drosophila
Popis výsledku anglicky
Adenosine (Ado) is an important signaling molecule involved in stress responses. Studies in mammalian models have shown that Ado regulates signaling mechanisms involved in ‘danger-sensing’ and tissue-protection. Yet, little is known about the role of Ado signaling in Drosophila. In the present study, we observed lower extracellular Ado concentration and suppressed expression of Ado transporters in flies expressing mutant huntingtin protein (mHTT). We altered Ado signaling using genetic tools and found that the overexpression of Ado metabolic enzymes, as well as the suppression of Ado receptor (AdoR) and transporters (ENTs), were able to minimize mHTT-induced mortality. We also identified the downstream targets of the AdoR pathway, the modifier of mdg4 (Mod(mdg4)) and heat-shock protein 70 (Hsp70), which carry out its function. Finally, we showed that a decrease in Ado signaling affect other Drosophila stress reactions, including paraquat and heat-shock treatments. Our study provides important insights into how Ado regulates stress responses in Drosophila.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
<a href="/cs/project/GJ19-13784Y" target="_blank" >GJ19-13784Y: Výzkum mechanismů regulace vrozené imunitní odpovědi pomocí proteinů podobných chitinázám</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2021
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Frontiers in Cell and Developmental Biology
ISSN
2296-634X
e-ISSN
2296-634X
Svazek periodika
9
Číslo periodika v rámci svazku
MAR 12
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
13
Strana od-do
651367
Kód UT WoS článku
000632876500001
EID výsledku v databázi Scopus
2-s2.0-85103311176