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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Anti-oxidative stress response in Drosophila melanogaster - The role of adipokinetic hormone and adenosine

ZEMANOVÁ, Milada January 2016 (has links)
In this thesis, the phenomena of the oxidative stress (OS) and anti oxidative stress responses in insects are described in a comprehensive review, and the outcomes of the experimental work are presented. The focus of the work was on defence reactions and their putative control by the adipokinetic hormone (AKH) and adenosine in the Drosophila melanogaster model. For this purpose, we studied the effect of the paraquat (oxidative stressor) treatment on adult flies and larvae carrying mutations in Akh (Akh1) and adenosine receptor (AdoR1) genes, and in both these genes together (Akh1 AdoR1 double mutant). The initial mortality tests revealed the double mutant Akh1 AdoR1 was more sensitive to OS than either of the single mutants. The AKH synthesis under the OS condition seems to be out of the gene expression control, since the increase of an AKH amount in CNS was not linked with the stimulation of Akh gene expression after a paraquat treatment. Further, the gene expression of the antioxidant enzyme glutathione S transferase D1 (GstD1) increased rapidly with OS, though the enzyme activity increased negligibly regardless of both the OS and mutations. Interestingly, the relative expression of GstD1 gene was minimal in the double Akh1 AdoR1 mutant; thus, it was concluded that both AKH and adenosine are employed in the GstD1 gene expression control. Similarly, AKH and adenosine seem to act in tandem in glutathione (GSH) regeneration, since the GSH level was significantly lower in all untreated deficient flies with the maximal effect in the Akh1 AdoR1 double mutant; accordingly, the reduction in the GSH level was enhanced by paraquat treatment. Altogether, the important roles of both AKH and adenosine in the anti oxidative stress response in D. melanogaster were demonstrated.
2

Etude de la modulation de la réponse cellulaire au stress oxydatif par les protéines VP24 des virus Marburg et Ebola / Study of modulation of anti-oxidative cellular response by VP24 proteins of Marburgvirus and Ebolavirus

Page, Audrey 10 January 2012 (has links)
Les virus Ebola (EBOV) et Marburg (MARV) causent des fièvres hémorragiques chez les primates, y compris l’homme. Le taux de létalité peut atteindre 90% et il n’existe ni vaccin ni traitement contre ces virus. En raison de leurs caractéristiques moléculaires communes, EBOV et MARV sont regroupés au sein de la famille des Filoviridae. Le virion est composé de 7 protéines, dont la VP24, qui joue un rôle important dans l’assemblage et la condensation des nucléocapsides, et pour EBOV, elle est également responsable de l’inhibition de la réponse à l’IFN. Des mutations dans la séquence protéique de VP24 sont impliquées dans le processus d’adaptation chez un nouvel hôte. La protéine VP24 d’EBOV est donc multifonctionnelle. Pour MARV, cette protéine ne semble pas porter les fonctions décrites pour la VP24 d’EBOV. Afin de comprendre le rôle de la VP24 de MARV, nous avons identifié ses partenaires cellulaires par un crible double-hybride en levures. Nous avons mis en évidence l’interaction entre Keap1 et la VP24 de MARV, et confirmé ce résultat en cellules mammifères. Keap1 est une protéine impliquée dans le contrôle de la réponse au stress oxydatif, car elle inhibe le facteur de transcription Nrf2, qui régule l’expression d’enzymes impliquées dans la réduction des ERO. Nos résultats montrent que le domaine de Keap1 liant la VP24 est le même que celui liant Nrf2, et que la VP24 de MARV active Nrf2 pour la synthèse de molécules anti-oxydantes. Nous avons enfin évalué l’impact de la VP24 de MARV sur ERR, une autre cible de Keap1, et mesuré l’activité Nrf2 au cours de l’infection par EBOV. Nos résultats montrent des effets opposés des VP24 d’ EBOV et de MARV sur l’activité de Nrf2. / Ebola (EBOV) and Marburgvirus (MARV) are responsible for severe hemorrhagic syndrome in primates, including humans. The lethality rate can reach 90%, and no vaccine or treatment is available to counteract these diseases. EBOV and MARV have similar genomic organization and thus are placed in a distinct family, Filoviridae. VP24 is one of the 7 structural proteins which form the virion and has been shown to play an important role in assembly and condensation of viral nucleocapsids. VP24 of EBOV is responsible for prevention of cellular response to IFN. Mutations in EBOV VP24 gene are necessary for the adaptation to a new host. EBOV VP24 thus acts as a multifunctional factor. Available data suggest that MARV VP24 is not implicated in either the counteraction of IFN response, or in the adaptation process. In order to discover new functions for VP24 of MARV, we searched for its interaction with cellular proteins, using a yeast-double hybrid approach. We discovered an interaction between MARV VP24 and Keap1 protein and further confirmed this interaction in mammalian cells. Keap1 is a cellular protein involved in intracellular detection of Reactive Oxygen Species (ROS) and in the control of oxidative stress response. It inhibits the Nrf2 transcription factor, which regulates expression of antioxidant enzymes. Our results indicate that Keap1 binding domain for VP24 is the same as the one involved in Nrf2 binding, resulting in activation of transcriptional activity of Nrf2. Impact of MARV VP24 on ERRa, another target of Keap1, was also measured, as well as Nrf2 activity during EBOV infection. Our results showed that VP24 of EBOV and MARV have opposite effect on Nrf2 activity.

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