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TCTP and CSN4 interact to control cell cycle progression and development in Arabidopsis thaliana

Abstract : While plants and animals largely diverge in several major aspects, some biological functions are highly conserved between these kingdoms. During organism development, the correct implementation of organs with unique shape, size and function is the result of coordinated cellular processes as cell proliferation and expansion. Translationally Controlled Tumor Protein (TCTP) is a highly conserved protein among all eukaryotes. TCTP mutation leads to embryo lethality, indicating that it is mandatory for organism development. Moreover, it has been shown that TCTP controls organ growth by regulating the G1/S transition and cell cycle progression both in plants and animals. In animals, the molecular pathways by which TCTP controls cell proliferation are well known. However, in plants, the mechanism implicating TCTP in the control of development and cell cycle is less understood. To better understand how TCTP controls cell proliferation and development in Arabidopsis thaliana, the putative TCTP interactors were identified. Among them, CSN4, a subunit of the COP9 signalosome complex (CSN) known to be involved in the control of CULLINS (CUL) neddylation status and CULLIN-RING ubiquitin ligases (CRLs) activity, was identified. Through their ubiquitination activity, CRL complexes are known to control the accumulation of mains cell cycle regulators as Cyclins or Kip Related Proteins. Thus, during my PhD, I studied the interaction between TCTP and CSN4, in order to evaluate if CSN complex could link TCTP to cell cycle control. I used genetic, cellular and biochemical approaches to demonstrate that TCTP and CSN4 interact in the cytoplasm. Phenotypic characterization of plants and cell cultures down- or overexpressing these genes demonstrated that TCTP and CSN4 interact genetically to control G1/S transition. In order to understand if the interaction between these two proteins could interfere with the CSN complex function, I characterized CUL1 neddylation status in transgenic lines misexpressing TCTP and CSN4. Loss of function of TCTP increases the non-neddylated CUL1 fraction, while overexpression of TCTP increases neddylated CUL1 form. These data show that TCTP interferes with the role of CSN complex in regulating CUL1 neddylation. Accordingly, our data suggest that TCTP controls cell cycle progression via controlling CSN deneddylation activity, and thus influencing CRL activity. In the last part of my PhD, I addressed if this role of TCTP is conserved in animals. I used biochemical approach to evaluate CUL1 neddylation in Drosophila melanogaster downregulated for dTCTP. My data show that Drosophila larvae knockdown for dTCTP also leads to an increase of non-neddylated CUL1 fraction. These data suggest that the mechanism by which TCTP/CSN4 regulate cell cycle, is likely conserved between Arabidopsis and Drosophila
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Léo Betsch. TCTP and CSN4 interact to control cell cycle progression and development in Arabidopsis thaliana. Other [q-bio.OT]. Université de Lyon, 2017. English. ⟨NNT : 2017LYSE1227⟩. ⟨tel-01967612⟩

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