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Contrôle de la stabilité de TIMELESS par un complexe ubiquitine ligase de type Culline-3 dans l’horloge circadienne de Drosophila melanogaster

Abstract : Most living organisms possess a circadian clock (24 hours period). This internal clockallows them to anticipate the daily changes (light, temperature) due to the rotation of theearth and consequently adapt their behavior and physiology. The molecular clock relies ontwo negative feedback loops that generate oscillations of the clock gene mRNA. A delaybetween the accumulation of the mRNAs and the proteins is required for the feedback loop,and is generated by post-translational modifications of PERIOD and TIMELESS. The proteinoscillations are controlled by their phosphorylation, ubiquitination and proteasomedependentdegradation. The ubiquitin ligase SCFSlmb induces the circadian degradation ofPER and TIM. SCFJetlag controls the light-dependent degradation of TIM, which is involved inthe resetting of the clock.In our study, we have identified Cul-3, as a new clock ubiquitin ligase that controlsTIM stability. Our results indicate that Cul-3 mostly controls the stability ofhypophosphorylated TIM, independently of PER, whereas SLMB controls the stability ofphosphorylated TIM. We propose a model where TIM oscillations are regulated by twoubiquitination process. Cul-3 delays the night accumulation of TIM, whereas Slmbprecipitates its degradation at the end of the night.
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Alexandre Dognon. Contrôle de la stabilité de TIMELESS par un complexe ubiquitine ligase de type Culline-3 dans l’horloge circadienne de Drosophila melanogaster. Neurosciences [q-bio.NC]. Université Paris Sud - Paris XI, 2011. Français. ⟨NNT : 2011PA11T008⟩. ⟨tel-00718638⟩

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