Sedimentology and wine, a cross road

Part of the Alps and the foreland basin will be crossed by our field trip. Limestone, gypsum, landslide siliceous carbonate pebbles and clay, marls carbonates and sandstone are composing the main terroirs of the tasted wines

An Integrin-Dependent Role of Pouch Endoderm in Hyoid Cartilage Development

Pharyngeal endoderm is essential for and can reprogram development of the head skeleton. Here we investigate the roles of specific endodermal structures in regulating craniofacial development. We have isolated an integrinα5 mutant in zebrafish that has region-specific losses of facial cartilages derived from hyoid neural crest cells. In addition, the cranial muscles that normally attach to the affected cartilage region and their associated nerve are secondarily reduced in integrinα5(−) animals. Earlier in development, integrinα5 mutants also have specific defects in the formation of the first pouch, an outpocketing of the pharyngeal endoderm. By fate mapping, we show that the cartilage regions that are lost in integrinα5 mutants develop from neural crest cells directly adjacent to the first pouch in wild-type animals. Furthermore, we demonstrate that Integrinα5 functions in the endoderm to control pouch formation and cartilage development. Time-lapse recordings suggest that the first pouch promotes region-specific cartilage development by regulating the local compaction and survival of skeletogenic neural crest cells. Thus, our results reveal a hierarchy of tissue interactions, at the top of which is the first endodermal pouch, which locally coordinates the development of multiple tissues in a specific region of the vertebrate face. Lastly, we discuss the implications of a mosaic assembly of the facial skeleton for the evolution of ray-finned fish

Regulation of integrin-mediated cellular responses through assembly of a CAS/Crk scaffold

AbstractThe molecular coupling of CAS and Crk in response to integrin activation is an evolutionary conserved signaling module that controls cell proliferation, survival and migration. However, when deregulated, CAS/Crk signaling also contributes to cancer progression and developmental defects in humans. Here we highlight recent advances in our understanding of how CAS/Crk complexes assemble in cells to modulate the actin cytoskeleton, and the molecular mechanisms that regulate this process. We discuss in detail the spatiotemporal dynamics of CAS/Crk assembly and how this scaffold recruits specific effector proteins that couple integrin signaling networks to the migration machinery of cells. We also highlight the importance of CAS/Crk signaling in the dual regulation of cell migration and survival mechanisms that operate in invasive cells during development and pathological conditions associated with cancer metastasis

ROLE COORDONNE DES INTEGRINES LORS DE LA MIGRATION DES CELLULES DES CRETES NEURALES IN VITRO ET REGULATION DE LEUR ACTIVATION PAR SONIC HEDGEHOG

LES CELLULES DES CRETES NEURALES (CCN) FONT PARTIES DES TYPES CELLULAIRES DE LA MOITIE DORSALE DU TUBE NEURAL QUI SONT INDUITS PAR LES MEMBRES DE LA FAMILLE DES TGF NOTAMMENT BMP4. SOUS LE CONTROLE DE BMP4, LES CCN ACQUIERENT PAR LA SUITE DES PROPRIETES LOCOMOTRICES TRANSITOIRES QUI LEUR PERMETTENT D'ENVAHIR DIFFERENTES ZONES EMBRYONNAIRES AFIN DE S'Y DIFFERENCIER. LEUR MIGRATION S'EFFECTUE GRACE A L'ACQUISITION D'INTEGRINES, RECEPTEURS DE LA MATRICE EXTRACELLULAIRE ENVIRONNANTE ET DONT LA FIBRONECTINE EST L'UN DES CONSTITUANTS MAJEURS. NOUS AVONS TOUT D'ABORD ETABLIT LE REPERTOIRE DES RECEPTEURS INTEGRINES DE LA FIBRONECTINE EXPRIMES PAR LES CCN. CELLES-CI NE PRESENTENT PAS MOINS DE SEPT INTEGRINES A LEUR SURFACE MAIS SEULES QUATRE D'ENTRE ELLES SEMBLENT DIRECTEMENT IMPLIQUEES DANS LA LOCOMOTION DES CCN SUR LA FIBRONECTINE. LES INTEGRINES V 1 ET 8 1 REGULENT L'ADHERENCE TANDIS QUE LES INTEGRINES 4 1, 8 1 ET V 3 CONTROLENT LA MIGRATION. IL SEMBLE QUE L'INTEGRINE 4 1 COORDONNE L'ACTIVITE DES AUTRES INTEGRINES FONCTIONNELLES, CECI QUEL QUE SOIT LE TYPE DE SUBSTRAT UTILISE ET PROBABLEMENT PAR L'INTERMEDIAIRE DE MOLECULES TRANSMEMBRANAIRES ASSOCIEES AUX INTEGRINES, LES TETRASPANINES CD81, CD82 ET CD151. LA POLARITE DORSOVENTRALE DU TUBE NEURAL EST LE RESULTAT DES ACTIVITES ANTAGONISTES DES BMP ET DE SONIC HEDGEHOG (SHH), L'INDUCTEUR DES TYPES CELLULAIRES VENTRAUX. NOUS AVONS EMIS L'HYPOTHESE QUE SHH CONSTITUAIT AUSSI UN SIGNAL ANTAGONISTE DE BMP4 LORS DE L'EMIGRATION DES CCN. EN EFFET, LES CCN EN PRESENCE DE SHH SONT INCAPABLES DE SE DEPLACER. CETTE INHIBITION DE LA MIGRATION PAR SHH N'EST PAS LE FAIT D'UNE MODIFICATION DE LA SPECIFICATION DES CCN NI D'UN CHANGEMENT DE LA POLARITE DU TUBE NEURAL. DE PLUS, LA PROLIFERATION ET LA SURVIE DES CCN NE SONT PAS ALTEREES. SHH N'AFFECTE PAR NON PLUS L'EXPRESSION DES CADHERINES, DE RHOB OU DES INTEGRINES INTERVENANT LORS DE L'EMIGRATION DES CCN. EN FAIT, SHH INACTIVE LES INTEGRINES ET CONTROLE AINSI L'ADHERENCE ET LA MIGRATION DES CCN VIA UNE SEQUENCE SPECIFIQUE ET DISTINCTE DE CELLE IMPLIQUEE DANS L'INDUCTION DES NEURONES. NOUS PROPOSONS QUE SHH N'EST PAS SEULEMENT IMPLIQUEE DANS LA SPECIFICATION DES NEURONES MAIS REGULE AUSSI LE CARACTERE MIGRATOIRE DES CELLULES DU TUBE NEURAL, REVELANT UN NOUVEAU ROLE POUR CETTE MOLECULE DANS LE CONTROLE DE LA MORPHOGENESE.ORSAY-PARIS 11-BU Sciences (914712101) / SudocSudocFranceF

Focal adhesion kinase is required for neural crest cell morphogenesis during mouse cardiovascular development

Neural crest cells (NCCs) participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Focal adhesion kinase (FAK) mediates signal transduction by integrin and growth factor receptors, each of which is important for normal cardiovascular development. To investigate the role of FAK in NCC morphogenesis, we deleted it in murine NCCs using Wnt1cre, yielding craniofacial and cardiovascular malformations resembling those observed in individuals with DiGeorge syndrome. In these mice, we observed normal cardiac NCC migration but reduced differentiation into smooth muscle within the aortic arch arteries and impaired cardiac outflow tract rotation, which resulted in a dextroposed aortic root. Moreover, within the conotruncal cushions, Fak-deficient NCCs formed a less organized mesenchyme, with reduced expression of perlecan and semaphorin 3C, and exhibited disorganized F-actin stress fibers within the aorticopulmonary septum. Additionally, absence of Fak resulted in reduced in vivo phosphorylation of Crkl and Erk1/2, components of a signaling pathway essential for NCC development. Consistent with this, both TGF-β and FGF induced FAK and Crkl phosphorylation in control but not Fak-deficient NCCs in vitro. Our results indicate that FAK plays an essential role in cardiac outflow tract development by promoting the activation of molecules such as Crkl and Erk1/2