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<dc:title xml:lang="en">Regulation of natural transdifferentiation in Caenorhabditis elegans by chromatin remodellers, environmental cues and stress responses</dc:title>
<dcterms:alternative xml:lang="fr">Régulation de la transdifférenciation naturelle chez Caenorhabditis elegans par les remodelleurs de la chromatine, les conditions environnementales et les réponses au stress</dcterms:alternative>
<dc:subject xml:lang="fr">Plasticité cellulaire</dc:subject>
<dc:subject xml:lang="fr">Transdifférenciation</dc:subject>
<dc:subject xml:lang="fr">Licensers</dc:subject>
<dc:subject xml:lang="fr">Remodellage de la chromatine</dc:subject>
<dc:subject xml:lang="fr">Alimentation</dc:subject>
<dc:subject xml:lang="fr">TORC1</dc:subject>
<dc:subject xml:lang="fr">Mitochondrie</dc:subject>
<dc:subject xml:lang="fr">Insuline</dc:subject>
<dc:subject xml:lang="en">Cellular plasticity</dc:subject>
<dc:subject xml:lang="en">Transdifferentiation</dc:subject>
<dc:subject xml:lang="en">Licensers</dc:subject>
<dc:subject xml:lang="en">Chromatin remodelling</dc:subject>
<dc:subject xml:lang="en">Food intake</dc:subject>
<dc:subject xml:lang="en">TORC1</dc:subject>
<dc:subject xml:lang="en">Mitochondria</dc:subject>
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<tef:elementdEntree autoriteExterne="273956876" autoriteSource="Sudoc">Plasticité cellulaire</tef:elementdEntree>
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<dcterms:abstract xml:lang="fr">Y-to-PDA est un exemple majeur de transdifférenciation naturelle chez C. elegans. Le changement d’identité cellulaire repose sur l’action d’une cassette de facteur de plasticité conservés. Dans cette étude, nous mettons en évidence l’existence d’un second mécanisme permettant le blocage de de certains facteurs de remodelage de la chromatine comme le DREAM ou le NuRD, qui protègent l’identité initiale. Ce second mécanisme est centré sur la protéine LIN-15A. Nos résultats suggèrent également que l’action de LIN-15A est très spécifique, et peut-être limitée à a cellule Y. Dans la deuxième partie, nous montrons que les fonctions de LIN-15A, et du seul facteur de remodelage de la chromatine au sein de la cassette de plasticité, EGL-27, deviennent dispensable en l’absence de nourriture. Nous avons identifié que la voie TORC1 était responsable de ce phénomène. De plus, nous avons trouvé qu’une réduction de la fonction mitochondriale permettait également de compenser la perte de l’un ou l’autre de ces facteurs. Enfin, nous avons démontré que ces deux phénomènes, privation de nourriture et réduction de la fonction mitochondriale fonctionnaient de manière indépendante. Comme ces deux phénomènes affectent des facteurs de remodelage de la chromatine agissant dans deux mécanismes différents, nos résultats suggèrent que des signaux environnementaux et physiologiques peuvent modifier l’état général de la chromatine dans les cellules différenciées et modifier leur plasticité.</dcterms:abstract>
<dcterms:abstract xml:lang="en">: Y-to-PDA is a prominent example of natural transdifferentiation occurring in C. elegans. A cassette of conserved plasticity factors is notably required for this switch of cellular identity. In this study, we show that a second pathway acts in parallel to these plasticity factors, in order to antagonise conserved chromatin remodelling complexes such as the DREAM and the NuRD, which safeguard the initial identity. This pathway relies on a factor named LIN-15A. Our results suggest that the control it exerts on these remodellers is restricted restricted to few cells, possibly to Y. In the second part of the study, we report that the requirements of LIN-15A, and of the sole chromatin remodeller from the plasticity cassette, EGL-27, can be bypassed by food deprivation. Our results demonstrate that the TORC1 signalling links food intake and cellular plasticity. In a second time, we also show that mitochondrial dysfunction has a similar effect on these two mutants. Importantly, we found that these two mechanisms act in parallel. As both of these mechanisms can bypass the requirements for two factors related to chromatin remodelling, and acting in independent pathways, our results suggest that both environmental and physiological cues can broadly impact the chromatin landscape of differentiated cells and impact their cellular plasticity.</dcterms:abstract>
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