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Search Results: 1 - 10 of 229633 matches for " Jo?l Bockaert "
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Homer1a-Dependent Crosstalk Between NMDA and Metabotropic Glutamate Receptors in Mouse Neurons
Federica Bertaso,Gautier Roussignol,Paul Worley,Jol Bockaert,Laurent Fagni,Fabrice Ango
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009755
Abstract: A large number of evidences suggest that group-I metabotropic glutamate receptors (mGluR1a, 1b, 1c, 5a, 5b) can modulate NMDA receptor activity. Interestingly, a physical link exists between these receptors through a Homer-Shank multi-protein scaffold that can be disrupted by the immediate early gene, Homer1a. Whether such a versatile link supports functional crosstalk between the receptors is unknown.
Plant Insecticide L-Canavanine Repels Drosophila via the Insect Orphan GPCR DmX
Christian Mitri,Laurent Soustelle,Bérénice Framery,Jol Bockaert,Marie-Laure Parmentier,Yves Grau
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000147
Abstract: For all animals, the taste sense is crucial to detect and avoid ingesting toxic molecules. Many toxins are synthesized by plants as a defense mechanism against insect predation. One example of such a natural toxic molecule is l-canavanine, a nonprotein amino acid found in the seeds of many legumes. Whether and how insects are informed that some plants contain l-canavanine remains to be elucidated. In insects, the taste sense relies on gustatory receptors forming the gustatory receptor (Gr) family. Gr proteins display highly divergent sequences, suggesting that they could cover the entire range of tastants. However, one cannot exclude the possibility of evolutionarily independent taste receptors. Here, we show that l-canavanine is not only toxic, but is also a repellent for Drosophila. Using a pharmacogenetic approach, we find that flies sense food containing this poison by the DmX receptor. DmXR is an insect orphan G-protein–coupled receptor that has partially diverged in its ligand binding pocket from the metabotropic glutamate receptor family. Blockade of DmXR function with an antagonist lowers the repulsive effect of l-canavanine. In addition, disruption of the DmXR encoding gene, called mangetout (mtt), suppresses the l-canavanine repellent effect. To avoid the ingestion of l-canavanine, DmXR expression is required in bitter-sensitive gustatory receptor neurons, where it triggers the premature retraction of the proboscis, thus leading to the end of food searching. These findings show that the DmX receptor, which does not belong to the Gr family, fulfills a gustatory function necessary to avoid eating a natural toxin.
Hyperfunction of Muscarinic Receptor Maintains Long-Term Memory in 5-HT4 Receptor Knock-Out Mice
Luis Segu,Marie-José Lecomte,Mathieu Wolff,Julie Santamaria,René Hen,Aline Dumuis,Sylvie Berrard,Jol Bockaert,Marie-Christine Buhot,Valérie Compan
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009529
Abstract: Patients suffering from dementia of Alzheimer's type express less serotonin 4 receptors (5-HTR4), but whether an absence of these receptors modifies learning and memory is unexplored. In the spatial version of the Morris water maze, we show that 5-HTR4 knock-out (KO) and wild-type (WT) mice performed similarly for spatial learning, short- and long-term retention. Since 5-HTR4 control mnesic abilities, we tested whether cholinergic system had circumvented the absence of 5-HTR4. Inactivating muscarinic receptor with scopolamine, at an ineffective dose (0.8 mg/kg) to alter memory in WT mice, decreased long-term but not short-term memory of 5-HTR4 KO mice. Other changes included decreases in the activity of choline acetyltransferase (ChAT), the required enzyme for acetylcholine synthesis, in the septum and the dorsal hippocampus in 5-HTR4 KO under baseline conditions. Training- and scopolamine-induced increase and decrease, respectively in ChAT activity in the septum in WT mice were not detected in the 5-HTR4 KO animals. Findings suggest that adaptive changes in cholinergic systems may circumvent the absence of 5-HTR4 to maintain long-term memory under baseline conditions. In contrast, despite adaptive mechanisms, the absence of 5-HTR4 aggravates scopolamine-induced memory impairments. The mechanisms whereby 5-HTR4 mediate a tonic influence on ChAT activity and muscarinic receptors remain to be determined.
Muscle Dystroglycan Organizes the Postsynapse and Regulates Presynaptic Neurotransmitter Release at the Drosophila Neuromuscular Junction
Laurent Bogdanik, Bérénice Framery, Andreas Fr?lich, Bénédicte Franco, Dominique Mornet, Jol Bockaert, Stephan J. Sigrist, Yves Grau, Marie-Laure Parmentier
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002084
Abstract: Background The Dystrophin-glycoprotein complex (DGC) comprises dystrophin, dystroglycan, sarcoglycan, dystrobrevin and syntrophin subunits. In muscle fibers, it is thought to provide an essential mechanical link between the intracellular cytoskeleton and the extracellular matrix and to protect the sarcolemma during muscle contraction. Mutations affecting the DGC cause muscular dystrophies. Most members of the DGC are also concentrated at the neuromuscular junction (NMJ), where their deficiency is often associated with NMJ structural defects. Hence, synaptic dysfunction may also intervene in the pathology of dystrophic muscles. Dystroglycan is a central component of the DGC because it establishes a link between the extracellular matrix and Dystrophin. In this study, we focused on the synaptic role of Dystroglycan (Dg) in Drosophila. Methodology/Principal Findings We show that Dg was concentrated postsynaptically at the glutamatergic NMJ, where, like in vertebrates, it controls the concentration of synaptic Laminin and Dystrophin homologues. We also found that synaptic Dg controlled the amount of postsynaptic 4.1 protein Coracle and alpha-Spectrin, as well as the relative subunit composition of glutamate receptors. In addition, both Dystrophin and Coracle were required for normal Dg concentration at the synapse. In electrophysiological recordings, loss of postsynaptic Dg did not affect postsynaptic response, but, surprisingly, led to a decrease in glutamate release from the presynaptic site. Conclusion/Significance Altogether, our study illustrates a conservation of DGC composition and interactions between Drosophila and vertebrates at the synapse, highlights new proteins associated with this complex and suggests an unsuspected trans-synaptic function of Dg.
Plant Insecticide L-Canavanine Repels Drosophila via the Insect Orphan GPCR DmX
Christian Mitri equal contributor,Laurent Soustelle equal contributor,Bérénice Framery,Jol Bockaert,Marie-Laure Parmentier,Yves Grau
PLOS Biology , 2009, DOI: 10.1371/journal.pbio.1000147
Abstract: For all animals, the taste sense is crucial to detect and avoid ingesting toxic molecules. Many toxins are synthesized by plants as a defense mechanism against insect predation. One example of such a natural toxic molecule is l-canavanine, a nonprotein amino acid found in the seeds of many legumes. Whether and how insects are informed that some plants contain l-canavanine remains to be elucidated. In insects, the taste sense relies on gustatory receptors forming the gustatory receptor (Gr) family. Gr proteins display highly divergent sequences, suggesting that they could cover the entire range of tastants. However, one cannot exclude the possibility of evolutionarily independent taste receptors. Here, we show that l-canavanine is not only toxic, but is also a repellent for Drosophila. Using a pharmacogenetic approach, we find that flies sense food containing this poison by the DmX receptor. DmXR is an insect orphan G-protein–coupled receptor that has partially diverged in its ligand binding pocket from the metabotropic glutamate receptor family. Blockade of DmXR function with an antagonist lowers the repulsive effect of l-canavanine. In addition, disruption of the DmXR encoding gene, called mangetout (mtt), suppresses the l-canavanine repellent effect. To avoid the ingestion of l-canavanine, DmXR expression is required in bitter-sensitive gustatory receptor neurons, where it triggers the premature retraction of the proboscis, thus leading to the end of food searching. These findings show that the DmX receptor, which does not belong to the Gr family, fulfills a gustatory function necessary to avoid eating a natural toxin.
Gαo Is Required for L-Canavanine Detection in Drosophila
Isabelle Devambez, Moutaz Ali Agha, Christian Mitri, Jol Bockaert, Marie-Laure Parmentier, Frédéric Marion-Poll, Yves Grau, Laurent Soustelle
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063484
Abstract: Taste is an essential sense for the survival of most organisms. In insects, taste is particularly important as it allows to detect and avoid ingesting many plant toxins, such as L-canavanine. We previously showed that L-canavanine is toxic for Drosophila melanogaster and that flies are able to detect this toxin in the food. L-canavanine is a ligand of DmXR, a variant G-protein coupled receptor (GPCR) belonging to the metabotropic glutamate receptor subfamily that is expressed in bitter-sensitive taste neurons of Drosophila. To transduce the signal intracellularly, GPCR activate heterotrimeric G proteins constituted of α, β and γ subunits. The aim of this study was to identify which Gα protein was required for L-canavanine detection in Drosophila. By using a pharmacological approach, we first demonstrated that DmXR has the best coupling with Gαo protein subtype. Then, by using genetic, behavioral assays and electrophysiology, we found that Gαo47A is required in bitter-sensitive taste neurons for L-canavanine sensitivity. In conclusion, our study revealed that Gαo47A plays a crucial role in L-canavanine detection.
Early administration of RS 67333, a specific 5-HT4 receptor agonist, prevents amyloidogenesis and behavioral deficits in the 5XFAD mouse model of Alzheimer’s disease
Patrizia Giannoni,Florence Gaven,Dimitri de Bundel,Kevin Baranger,Evelyne Marchetti-Gauthier,Fran?ois S. Roman,Emmanuel Valjent,Philippe Marin,Jol Bockaert,Santiago Rivera,Sylvie Claeysen
Frontiers in Aging Neuroscience , 2013, DOI: 10.3389/fnagi.2013.00096
Abstract: Amyloid β (Aβ) accumulation is considered the main culprit in the pathogenesis of Alzheimer’s disease (AD). Recent studies suggest that decreasing Aβ production at very early stages of AD could be a promising strategy to slow down disease progression. Serotonin 5-HT4 receptor activation stimulates α-cleavage of the amyloid precursor protein (APP), leading to the release of the soluble and neurotrophic sAPPα fragment and thus precluding Aβ formation. Using the 5XFAD mouse model of AD that shows accelerated Aβ deposition, we investigated the effect of chronic treatments (treatment onset at different ages and different durations) with the 5-HT4 receptor agonist RS 67333 during the asymptomatic phase of the disease. Chronic administration of RS 67333 decreased concomitantly the number of amyloid plaques and the level of Aβ species. Reduction of Aβ levels was accompanied by a striking decrease in hippocampal astrogliosis and microgliosis. RS 67333 also transiently increased sAPPα concentration in the cerebrospinal fluid and brain. Moreover, a specific 5-HT4 receptor antagonist (RS 39604) prevented the RS 67333-mediated reduction of the amyloid pathology. Finally, the novel object recognition test deficits of 5XFAD mice were reversed by chronic treatment with RS 67333. Collectively, these results strongly highlight this 5-HT4 receptor agonist as a promising disease modifying-agent for AD.
Systems medicine and integrated care to combat chronic noncommunicable diseases
Jean Bousquet, Josep M Anto, Peter J Sterk, Ian M Adcock, Kian Chung, Josep Roca, Alvar Agusti, Chris Brightling, Anne Cambon-Thomsen, Alfredo Cesario, Sonia Abdelhak, Stylianos E Antonarakis, Antoine Avignon, Andrea Ballabio, Eugenio Baraldi, Alexander Baranov, Thomas Bieber, Jol Bockaert, Samir Brahmachari, Christian Brambilla, Jacques Bringer, Michel Dauzat, Ingemar Ernberg, Leonardo Fabbri, Philippe Froguel, David Galas, Takashi Gojobori, Peter Hunter, Christian Jorgensen, Francine Kauffmann
Genome Medicine , 2011, DOI: 10.1186/gm259
Abstract: Chronic diseases are disorders of long duration and generally slow progression [1]. They include four major non-communicable diseases (NCDs) listed by the World Health Organization (WHO) [2] - cardiovascular diseases, cancer, chronic respiratory diseases and diabetes - as well as other NCDs, such as neuropsychiatric disorders [3] and arthritis. As survival rates have improved for infectious and genetic diseases, chronic diseases have come to include communicable diseases (such as HIV/AIDS) and genetic disorders (such as cystic fibrosis). NCDs represent the major global health problem of the 21st century [4,5]; they affect all age groups [6] and their burden is greater than that of infectious diseases. NCDs are the world leading cause of disease burden and mortality [2] and are increasing in prevalence and burden [7], even in low- and middle-income countries [8]. Costs incurred by uncontrolled NCDs are substantial, especially in underserved populations [9] and low- and middle-income countries [10,11]. NCDs are an under-appreciated cause of poverty and hinder economic development [11]. Importantly, management of NCDs has recently been prioritized globally (Box 1).Chronic diseases are caused by complex gene-environment interactions acting across the lifespan from the fetus to old age (Figure 1). In this context, 'environment' includes risk and protective factors associated with environment and lifestyle, such as tobacco, nutrition, indoor and outdoor air pollution and sedentary life [2].Socio-economic determinants are intertwined with the onset, progression, severity and control of NCDs. There are functional interdependencies between molecular components, reflecting complex network perturbations that link cells, tissues and organs [12]. Early life events are crucial in the generation of NCDs, and aging increases disease complexity, adding, for example, tissue and cell senescence [13]. Comorbidity refers to the co-existence of two or more diseases or conditions in the s
Convergence of formal invertible CR mappings between minimal holomorphically nondegenerate real analytic hypersurfaces
Jo l Merker
International Journal of Mathematics and Mathematical Sciences , 2001, DOI: 10.1155/s0161171201020117
Abstract: Recent advances in CR (Cauchy-Riemann) geometry have raised interesting fine questions about the regularity of CR mappings between real analytic hypersurfaces. In analogy with the known optimal results about the algebraicity of holomorphic mappings between real algebraic sets, some statements about the optimal regularity of formal CR mappings between real analytic CR manifolds can be naturally conjectured. Concentrating on the hypersurface case, we show in this paper that a formal invertible CR mapping between two minimal holomorphically nondegenerate real analytic hypersurfaces in ℂn is convergent. The necessity of holomorphic nondegeneracy was known previously. Our technique is an adaptation of the inductional study of the jets of formal CR maps which was discovered by Baouendi-Ebenfelt-Rothschild. However, as the manifolds we consider are far from being finitely nondegenerate, we must consider some new conjugate reflection identities which appear to be crucial in the proof. The higher codimensional case will be studied in a forthcoming paper.
Targeting and Anchoring Tudor in the Pole Plasm of the Drosophila Oocyte
Jol Anne
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0014362
Abstract: Germline formation is a highly regulated process in all organisms. In Drosophila embryos germ cells are specified by the pole plasm, a specialized cytoplasmic region containing polar granules. Components of these granules are also present in the perinuclear ring surrounding nurse cells, the nuage. Two such molecules are the Vasa and Tudor proteins. How Tudor localizes and is maintained in the pole plasm is, however, not known.
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