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<dc:title xml:lang="en">Analysis of the local mechanisms that prime cells for natural transdifferentiation in vivo</dc:title>
<dcterms:alternative xml:lang="fr">Analyse des mécanismes locaux qui rendent une cellule susceptible de subir une transdifférenciation naturelle in vivo</dcterms:alternative>
<dc:subject xml:lang="fr">Notch</dc:subject>
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<dc:subject xml:lang="fr">Ascl1</dc:subject>
<dc:subject xml:lang="fr">Hlh-14</dc:subject>
<dc:subject xml:lang="fr">Transdifférenciation</dc:subject>
<dc:subject xml:lang="fr">Reprogrammation</dc:subject>
<dc:subject xml:lang="fr">Plasticité cellulaire</dc:subject>
<dc:subject xml:lang="fr">Identité cellulaire</dc:subject>
<dc:subject xml:lang="fr">Diversification cellulaire</dc:subject>
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<dcterms:abstract xml:lang="fr">L’étude porte sur les mécanismes qui permettent à certaines cellules de changer d’identité, étudiés in vivo et à l’échelle de la cellule unique chez C. elegans. Elle s’appuie sur deux modèles naturels de conversion épithélium-neurone, Y-to-PDA et K-to-DVB, afin de comprendre pourquoi certaines cellules sont capables de se reprogrammer alors que d’autres ne le sont pas. Les résultats montrent que la voie Notch confère l’identité Y ainsi que sa compétence à se reprogrammer, tandis qu’une activation prolongée bloque cette plasticité. Ils identifient également hlh-14/Ascl1, comme un facteur clé dont le rôle dépend du contexte : il restreint le nombre d’événements Y-to-PDA en orientant les progéniteurs vers un destin neuronal DA9, mais il est requis pour la conversion K-to-DVB et suffit à induire des conversions ectopiques en DVB lorsqu’il est surexprimé. Ces travaux éclairent la manière dont signaux extrinsèques et facteurs intrinsèques s’articulent pour contrôler la plasticité cellulaire.</dcterms:abstract>
<dcterms:abstract xml:lang="en">This study investigates the mechanisms that allow certain cells to change identity, examined in vivo and at the single-cell level in C. elegans. It is based on two natural models of epithelium-to-neuron conversion, Y-to-PDA and K-to-DVB, in order to understand why some cells are able to reprogram whereas others are not. The results show that the Notch pathway confers Y identity as well as the competence to reprogram, whereas prolonged activation blocks this plasticity. They also identify hlh-14/Ascl1 as a key factor whose role depends on the context: it restricts the number of Y-to-PDA events by redirecting progenitors toward a DA9 neuronal fate, but it is required for K-to-DVB conversion and is sufficient to induce ectopic DVB conversions when overexpressed. This work sheds light on how extrinsic signals and intrinsic factors interact to control cellular plasticity.</dcterms:abstract>
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