Durant ce travail de thèse, nous nous sommes efforcés d’étudier la fonction des protéines VIT32 et RGS2 dans le contexte de l’organisme. Cette approche a été motivée premièrement par l’observation du fait que le transport de sodium engendré par l’activation de la voie des MAPK dépend de protéines différentes selon le système in vitro étudié. Deuxièmement, le grand nombre et la diversité des fonctions attribuées à RGS2 in vitro laissent supposer que certaines d’entre elles ne reflètent pas forcément la situation rencontrée dans l’organisme entier.
Dans cette optique, nous avons commencé à générer une souris VIT32 KO conditionnel. Malgré le fait que la plupart des étapes aient été franchies, il nous manque encore l’étape ultime de la transmission de l’allèle floxé à la descendance des souris chimériques. Cela illustre une difficulté majeure de l’établissement d’une étude in vivo : elle comprend un grand nombre d’étapes et même si celles‐ci sont bien planifiées au préalable, elles comportent souvent des difficultés inattendues. Il faut donc passer beaucoup de temps à optimiser les conditions expérimentales afin de franchir ces obstacles.
En parallèle, nous avons étudié le phénotype rénal de souris RGS2 KO. Cette partie du travail de thèse a mis en évidence un autre aspect de la difficulté à travailler sur un organisme entier. En effet, il n’a pas été facile de mettre à jour la fonction de RGS2 dans le contexte de l’animal, probablement en raison des mécanismes de compensation qui s’établissent suite à la délétion d’un gène. En outre, des modifications phénotypiques subtiles sont difficiles à percevoir étant donné les fortes variations individuelles et le faible nombre d’individus sur lesquels il est possible de travailler.
Néanmoins, nous sommes parvenus à attribuer un rôle à RGS2 dans la rétroaction négative de la voie de signalisation de la vasopressine dans les tubules rénaux. Cela constitue un pas important à la compréhension du mécanisme complexe de la régulation fine de la concentration urinaire. A long terme, on peut envisager que RGS2 soit une cible thérapeutique pour traiter des problèmes liés à la réabsorption d’eau.
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