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1. miR-34/449 control apical actin network formation during multiciliogenesis through small GTPase pathways

Author

Chevalier B, Adamiok A, Mercey O, Dr, Revinski, Le, Zaragosi, Pasini A, Kodjabachian L, Pascal Barbry, Marcet B, Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), ANR-11-LABX-0028,SIGNALIFE,Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie(2011), ANR-18-INBS-0001,France Génomique CREFIX,Utilisation des fonds du centre de référence d'innovation et d'expertise (CREFIX) du plan de médecine génomique (PFMG 2025)(2018), ANR-09-GENO-0039,MERCI,Rôle des microARNs dans la différenciation de l'épithélium respiratoire humain normal et pathologique(2009), ANR-11-BSV2-0021,COMMIT,Contrôle de la multiciliogénèse motile chez les tétrapodes(2011), ANR-12-EMMA-0015,MITHRA,Les microARN, alternative thérapeutique dans l'Asthme(2012), ANR-10-INBS-0004,France-BioImaging,Développment d'une infrastructure française distribuée coordonnée(2010), Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)

Subjects
Embryo, Nonmammalian, Filamins, [SDV]Life Sciences [q-bio], Small GTPases, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, macromolecular substances, Real-Time Polymerase Chain Reaction, Article, Ectopic Gene Expression, Xenopus laevis, Animals, Humans, Cilia, In Situ Hybridization, Actin, Monomeric GTP-Binding Proteins, Microscopy, Confocal, Ciliogenesis, Endothelial Cells, Epithelial Cells, Immunohistochemistry, Actins, Basal Bodies, Africa, Western, MicroRNAs, Nasal Mucosa, miRNAs, ras Proteins
Abstract

Vertebrate multiciliated cells (MCCs) contribute to fluid propulsion in several biological processes. We previously showed that microRNAs of the miR-34/449 family trigger MCC differentiation by repressing cell cycle genes and the Notch pathway. Here, using human and Xenopus MCCs, we show that beyond this initial step, miR-34/449 later promote the assembly of an apical actin network, required for proper basal bodies anchoring. Identification of miR-34/449 targets related to small GTPase pathways led us to characterize R-Ras as a key regulator of this process. Protection of RRAS messenger RNA against miR-34/449 binding impairs actin cap formation and multiciliogenesis, despite a still active RhoA. We propose that miR-34/449 also promote relocalization of the actin binding protein Filamin-A, a known RRAS interactor, near basal bodies in MCCs. Our study illustrates the intricate role played by miR-34/449 in coordinating several steps of a complex differentiation programme by regulating distinct signalling pathways., MicroRNAs of the miR-34/449 family initiate formation of multiciliated cells through the suppression of cell cycle genes and Notch. Here the authors show that miR-34/449 also regulate the assembly of an apical actin network necessary for basal body anchoring by regulating the expression of R-Ras.

Published
2015
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2. Functional expression of two olfactory receptors in the Baculovirus/insect system

Author

Clos-Faybesse, Olivier, Matarazzo, V., Marcet, B., Guiraudie-Capraz, G., Devauchelle, G., Etievant, P., Cerutti, M., Ronin, C., Neurobiologie intégrative et adaptative (NIA), and Université de Provence - Aix-Marseille 1-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
Published
2005

3. General anesthetic octanol and related compounds activate wild-type and delF508 cystic fibrosis chloride channels

Author

Marcet, B., Becq, F., Norez, C., Delmas, P., Verrier, Bernard, Plasticité et physio-pathologie de la motricité (P3M) (PPPMP), Centre National de la Recherche Scientifique (CNRS)-Université de la Méditerranée - Aix-Marseille 2, Université de la Méditerranée - Aix-Marseille 2-Centre National de la Recherche Scientifique (CNRS), and Ruemgardt, Joelle

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Octanols, Patch-Clamp Techniques, Cystic Fibrosis, fungi, Cystic Fibrosis Transmembrane Conductance Regulator, Epithelial Cells, CHO Cells, respiratory system, Cyclic AMP-Dependent Protein Kinases, digestive system diseases, respiratory tract diseases, Cell Line, Chloride Channels, Cricetinae, Papers, Cyclic AMP, Animals, Humans, Calcium, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Hydrophobic and Hydrophilic Interactions
Abstract

1. Cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel is defective during cystic fibrosis (CF). Activators of the CFTR Cl(-) channel may be useful for therapy of CF. Here, we demonstrate that a range of general anesthetics like normal-alkanols (n-alkanols) and related compounds can stimulate the Cl(-) channel activity of wild-type CFTR and delF508-CFTR mutant. 2. The effects of n-alkanols like octanol on CFTR activity were measured by iodide ((125)I) efflux and patch-clamp techniques on three distinct cellular models: (1). CFTR-expressing Chinese hamster ovary cells, (2). human airway Calu-3 epithelial cells and (3). human airway JME/CF15 epithelial cells which express the delF508-CFTR mutant. 3. Our data show for the first time that n-alkanols activate both wild-type CFTR and delF508-CFTR mutant. Octanol stimulated (125)I efflux in a dose-dependent manner in CFTR-expressing cells (wild-type and delF508) but not in cell lines lacking CFTR. (125)I efflux and Cl(-) currents induced by octanol were blocked by glibenclamide but insensitive to 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid, as expected for a CFTR Cl(-) current. 4. CFTR activation by octanol was neither due to cell-to-cell uncoupling properties of octanol nor to an intracellular cAMP increase. CFTR activation by octanol requires phosphorylation by protein kinase-A (PKA) since it was prevented by H-89, a PKA inhibitor. 5. n-Alkanols chain length was an important determinant for channel activation, with rank order of potencies: 1-heptanol1-octanol2-octanol1-decanol. Our findings may be of valuable interest for developing novel therapeutic strategies for CF.

Published
2004

4. MICRORNAS AS NEW PLAYERS OF INFLAMMATION

Author

Mari, B., Rezzonicco, R., Zaragosi, L. E., Pottier, N., Marcet, B., Chevalier, B., Bertero, T., Puissegur, M. P., Grosso, S., Robbe-Sermesant, K., Lebrigand, K., Rios, G., Fourre, S., Magnone, V., Ponzio, G., Rainer Waldmann, and Barbry, P.

5. [MicroRNA control biosynthesis of motile cilia in vertebrates]

Author

Chevalier B, Kodjabachian L, Coraux C, Pascal Barbry, Marcet B, Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Plasticité de l'épithélium respiratoire dans les conditions normales et pathologiques - UMR-S 903 (PERPMP), SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre Hospitalier Universitaire de Reims (CHU Reims)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Reims Champagne-Ardenne (URCA), Université Nice Sophia Antipolis (1965 - 2019) (UNS), Université de Reims Champagne-Ardenne (URCA)-Centre Hospitalier Universitaire de Reims (CHU Reims)-Institut National de la Santé et de la Recherche Médicale (INSERM)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), and Université de Reims Champagne-Ardenne (URCA)-Université de Reims Champagne-Ardenne (URCA)

Subjects
MESH: Cystic Fibrosis, Bronchi/cytology/secretion, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH: Receptor, Notch1, MESH: Gene Expression Profiling, Xenopus laevis, Epithelial Cells/secretion/ultrastructure, MESH: Xenopus laevis, MESH: Cilia, MicroRNAs/genetics/*physiology, MESH: Intracellular Signaling Peptides and Proteins, MESH: Mucus, Mucus/secretion, Cell Movement/genetics, Vertebrates/*genetics, Animals, Humans, MESH: Animals, MESH: Vertebrates, MESH: Cell Movement, ComputingMilieux_MISCELLANEOUS, Intracellular Signaling Peptides and Proteins/physiology, MESH: Humans, Cystic Fibrosis/pathology, Nonmammalian, Notch1/physiology, Gene Expression Profiling, Membrane Proteins/physiology, MESH: Bronchi, MESH: Embryo, Nonmammalian, MESH: Epithelial Cells, Embryo, MESH: Membrane Proteins, Cilia/*genetics/metabolism, MESH: Epidermis, Epidermis/embryology/secretion/ultrastructure, MESH: MicroRNAs, Receptor
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