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  E-mail Message: I thought you might be interested in this item at http://www.worldcat.org/oclc/898009144 Title: Regulation of the growth of the myocardium in the developing mouse and characterization of the role of Fat4 in the control of heart size Author: Chiara Ragni; Sigolène Meilhac; Université Pierre et Marie Curie (Paris / 1971-2017); École doctorale Complexité du vivant (Paris) Publisher: 2014. OCLC:898009144

  
  

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Regulation of the growth of the myocardium in the developing mouse and characterization of the role of Fat4 in the control of heart size

Author:	Chiara Ragni; Sigolène Meilhac; Université Pierre et Marie Curie (Paris / 1971-2017).; École doctorale Complexité du vivant (Paris).
Publisher:	2014.
Dissertation:	Thèse de doctorat : Biologie du développement : Paris 6 : 2014.
Edition/Format:	Computer file : Document : Thesis/dissertation : English
Summary:	Dans ce travail, nous nous sommes intéressés à caractériser la polarité et la croissance du myocarde au cours du développement de la souris. Travaux antérieurs ont montré que la croissance du myocarde est orientée. Cependant, les processus qui sous-tendent cette croissance orientée restent mal connus. Dans d'autres systèmes, la polarité des cellules régule plusieurs comportements cellulaires. Suivant cette hypothèse, nous montrons que la polarité et la division des cellules du myocarde sont coordonnée dans le cœur embryonnaire. Notre objectif suivant était d'obtenir des indications fonctionnelles sur les signaux de croissance du myocarde. Dans le cœur, la voie de la Polarité Cellulaire Planaire (PCP) ainsi que la voie Hippo sont requises pour sa morphogenèse. Chez la mouche, la cadhérine atypique Fat module les voies PCP et Hippo. Le rôle de Fat4, l'orthologue chez les mammifères, comme régulateur de la voie Hippo est controversé. En utilisant les mutants Fat4, nous montrons que Fat4 module la croissance du myocarde plutôt que sa polarité. A la naissance, les mutants Fat4 ont des parois ventriculaires plus épaisses, associées à une prolifération accrue des cardiomyocytes. Nous montrons aussi que Fat4 module l'activité de Yap1, l'effecteur principal de la voie Hippo dans le cœur. Néanmoins, contrairement à la mouche, nous apportons ici la preuve que Fat4 module Yap1 d'une manière non-canonique, en impliquant l'adaptator Amotl1. Ainsi, nous proposons un modèle dans lequel, lorsque Fat4 est supprimé, Amotl1 rentre dans le noyau avec Yap1 pour promouvoir la prolifération des cardiomyocytes. Nos résultats ouvrent des perspectives importantes pour la réparation du cœur blessé. For this work, we focussed on characterizing myocardial polarity and growth during mouse development. Previous work, showed that the growth of the myocardium is oriented. However, which processes underly such oriented growth has remained unclear. In other systems, cell polarity regulates several types of oriented cell behaviour. Following this hypothesis, we show that myocardial cell polarity and division are coordinated in the embryonic heart. Next, we aimed to gain functional insights into the signals required for the growth of the myocardium. In the heart, both Planar Cell Polarity (PCP) and Hippo signalling are required for proper morphogenesis. In the fruit fly, the atypical cadherin Fat modulates both PCP and the Hippo pathways. The mammalian ortholog Fat4 regulates PCP in the kidneys and in the inner ear. However, its role as an upstream regulator of the Hippo pathway is controversial. Using Fat4 mutants, we show that Fat4 modulates myocardial growth rather than polarity. At birth, Fat4 mutants have thicker myocardial walls and this is associated with increased cardiomyocyte proliferation. Mechanistically, we show that Fat4 modulates the activity of Yap1, the main downstream effector of the Hippo pathway in the heart. However, contrary to the fruit fly, we provide novel evidence that Fat4 modulates Yap1 in a non-canonical way, that implies the adaptor protein Amotl1. Thus, we propose a model where, upon suppression of Fat4, Amotl1 translocates into the nucleus with Yap1 to promote myocardial cell proliferation. Our findings open important perspectives for the repair of the injuried heart, as Fat4 and its effector Amotl1 might play important roles in this context.  Read more...
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Subjects	Myocarde. Cadhérines. Coeur View all subjects
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