Institute Of Biologie Of Lecole Normale Superieure

Le Touquet – Paris-Plage, France

Institute Of Biologie Of Lecole Normale Superieure

Le Touquet – Paris-Plage, France
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Proville R.D.,Institute Of Biologie Of Lecole Normale Superieure | Proville R.D.,French National Center for Scientific Research | Proville R.D.,French Institute of Health and Medical Research | Spolidoro M.,Institute Of Biologie Of Lecole Normale Superieure | And 18 more authors.
Nature Neuroscience | Year: 2014

Sensorimotor integration is crucial to perception and motor control. How and where this process takes place in the brain is still largely unknown. Here we analyze the cerebellar contribution to sensorimotor integration in the whisker system of mice. We identify an area in the cerebellum where cortical sensory and motor inputs converge at the cellular level. Optogenetic stimulation of this area affects thalamic and motor cortex activity, alters parameters of ongoing movements and thereby modifies qualitatively and quantitatively touch events against surrounding objects. These results shed light on the cerebellum as an active component of sensorimotor circuits and show the importance of sensorimotor cortico-cerebellar loops in the fine control of voluntary movements. © 2014 Nature America, Inc. All rights reserved.


Coulpier F.,Institute Of Biologie Of Lecole Normale Superieure | Decker L.,Institute Of Biologie Of Lecole Normale Superieure | Funalot B.,University of Limoges | Vallat J.-M.,University of Limoges | And 3 more authors.
Journal of Neuroscience | Year: 2010

CNS/PNS interfaces constitute cell boundaries, because they delimit territories with different neuronal and glial contents. Despite their potential interest in regenerative medicine, the mechanisms restricting oligodendrocytes and astrocytes to the CNS and Schwann cells to the PNS in mammals are not known. To investigate the involvement of peripheral glia and myelin in the maintenance of the CNS/PNS boundary, we have first made use of different mouse mutants. We show that depletion of Schwann cells and boundary cap cells or inactivation of Krox20/Egr2, a master regulatory gene for myelination in Schwann cells, results in transgression of the CNS/PNS boundary by astrocytes and oligodendrocytes and in myelination of nerve root axons by oligodendrocytes. In contrast, such migration does not occur with the TremblerJ mutation, which prevents PNS myelination without affecting Krox20 expression. Altogether, these data suggest that maintenance of the CNS/PNS boundary requires a Krox20 function separable from myelination control. Finally, we have analyzed a human patient affected by a congenital amyelinating neuropathy, associated with the absence of the KROX20 protein in Schwann cells. In this case, the nerve roots were also invaded by oligodendrocytes and astrocytes. This indicates that transgression of the CNS/PNS boundary by central glia can occur in pathological situations in humans and suggests that the underlying mechanisms are common with the mouse. Copyright©2010 the authors.


Berger N.,French National Institute for Agricultural Research | Dubreucq B.,French National Institute for Agricultural Research | Roudier F.,Institute Of Biologie Of Lecole Normale Superieure | Dubos C.,French National Institute for Agricultural Research | Lepiniec L.,French National Institute for Agricultural Research
Plant Cell | Year: 2011

LEAFY COTYLEDON2 (LEC2) is a master regulator of seed development in Arabidopsis thaliana. In vegetative organs, LEC2 expression is negatively regulated by Polycomb Repressive Complex2 (PRC2) that catalyzes histone H3 Lys 27 trimethylation (H3K27me3) and plays a crucial role in developmental phase transitions. To characterize the cis-regulatory elements involved in the transcriptional regulation of LEC2, molecular dissections and functional analyses of the promoter region were performed in vitro, both in yeast and in planta. Two cis-activating elements and a cis-repressing element (RLE) that is required for H3K27me3 marking were characterized. Remarkably, insertion of the RLE cis-element into pF3H, an unrelated promoter, is sufficient for repressing its transcriptional activity in different tissues. Besides improving our understanding of LEC2 regulation, this study provides important new insights into the mechanisms underlying H3K27me3 deposition and PRC2 recruitment at a specific locus in plants. © American Society of Plant Biologists. All rights reserved.


Segalen M.,French Institute of Health and Medical Research | Johnston C.A.,University of Oregon | Martin C.A.,French Institute of Health and Medical Research | Dumortier J.G.,Institute Of Biologie Of Lecole Normale Superieure | And 6 more authors.
Developmental Cell | Year: 2010

The Frizzled receptor and Dishevelled effector regulate mitotic spindle orientation in both vertebrates and invertebrates, but how Dishevelled orients the mitotic spindle is unknown. Using the Drosophila S2 cell " induced polarity" system, we find that Dishevelled cortical polarity is sufficient to orient the spindle and that Dishevelled's DEP domain mediates this function. This domain binds a C-terminal domain of Mud (the Drosophila NuMA ortholog), and Mud is required for Dishevelled-mediated spindle orientation. In Drosophila, Frizzled-Dishevelled planar cell polarity (PCP) orients the sensory organ precursor (pI) spindle along the anterior-posterior axis. We show that Dishevelled and Mud colocalize at the posterior cortex of pI, Mud localization at the posterior cortex requires Dsh, and Mud loss-of-function randomizes spindle orientation. During zebrafish gastrulation, the Wnt11-Frizzled-Dishevelled PCP pathway orients spindles along the animal-vegetal axis, and reducing NuMA levels disrupts spindle orientation. Overall, we describe a Frizzled-Dishevelled-NuMA pathway that orients division from Drosophila to vertebrates. © 2010 Elsevier Inc.


Nakajima K.,Kwansei Gakuin University | Tanaka A.,Kwansei Gakuin University | Tanaka A.,Institute Of Biologie Of Lecole Normale Superieure | Matsuda Y.,Kwansei Gakuin University
Proceedings of the National Academy of Sciences of the United States of America | Year: 2013

Photosynthesis in marine diatoms is a vital fraction of global primary production empowered by CO2-concentrating mechanisms. Acquisition of HCO3 - from seawater is a critical primary step of the CO2-concentrating mechanism, allowing marine photoautotrophic eukaryotes to overcome CO2 limitation in alkaline high-salinity water. However, little is known about molecular mechanisms governing this process. Here, we show the importance of a plasma membrane-type HCO 3 - transporter for CO2 acquisition in a marine diatom. Ten putative solute carrier (SLC) family HCO3 - transporter genes were found in the genome of the marine pennate diatom Phaeodactylum tricornutum. Homologs also exist in marine centric species, Thalassiosira pseudonana, suggesting a general occurrence of SLC transporters in marine diatoms. Seven genes were found to encode putative mammalian-type SLC4 family transporters in P. tricornutum, and three of seven genes were specifically transcribed under low CCO2 conditions. One of these gene products, PtSLC4-2, was localized at the plasmalemma and significantly stimulated both dissolved inorganic carbon (DIC) uptake and photosynthesis in P. tricornutum. DIC uptake by PtSLC4-2 was efficiently inhibited by an anion-exchanger inhibitor, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, in a concentration-dependent manner and highly dependent on Na+ ions at concentrations over 100 mM. These results show that DIC influx into marine diatoms is directly driven at the plasmalemma by a specific HCO3 - transporter with a significant halophilic nature.


Chazal P.-E.,French National Center for Scientific Research | Chazal P.-E.,Institute Of Biologie Of Lecole Normale Superieure | Daguenet E.,Institute Of Genetique Et Of Biologie Moleculaire Et Cellulaire | Daguenet E.,French National Center for Scientific Research | And 8 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2013

The multiprotein exon junction complex (EJC), deposited by the splicing machinery, is an important constituent of messenger ribonucleoprotein particles because it participates to numerous steps of the mRNA lifecycle from splicing to surveillance via nonsense-mediated mRNA decay pathway. By an unknown mechanism, the EJC also stimulates translation efficiency of newly synthesized mRNAs. Here, we show that among the four EJC core components, the RNA-binding protein metastatic lymph node 51 (MLN51) is a translation enhancer. Overexpression of MLN51 preferentially increased the translation of intron-containing reporters via the EJC, whereas silencing MLN51 decreased translation. In addition, modulation of the MLN51 level in cell-free translational extracts confirmed its direct role in protein synthesis. Immunoprecipitations indicated that MLN51 associates with translation-initiating factors and ribosomal subunits, and in vitro binding assays revealed that MLN51, alone or as part of the EJC, interacts directly with the pivotal eukaryotic translation initiation factor eIF3. Taken together, our data define MLN51 as a translation activator linking the EJC and the translation machinery.


Deleris A.,University of California at Los Angeles | Deleris A.,Institute Of Biologie Of Lecole Normale Superieure | Stroud H.,University of California at Los Angeles | Bernatavichute Y.,University of California at Los Angeles | And 5 more authors.
PLoS Genetics | Year: 2012

Dimethylation of histone H3 lysine 9 (H3K9m2) and trimethylation of histone H3 lysine 27 (H3K27m3) are two hallmarks of transcriptional repression in many organisms. In Arabidopsis thaliana, H3K27m3 is targeted by Polycomb Group (PcG) proteins and is associated with silent protein-coding genes, while H3K9m2 is correlated with DNA methylation and is associated with transposons and repetitive sequences. Recently, ectopic genic DNA methylation in the CHG context (where H is any base except G) has been observed in globally DNA hypomethylated mutants such as met1, but neither the nature of the hypermethylated loci nor the biological significance of this epigenetic phenomenon have been investigated. Here, we generated high-resolution, genome-wide maps of both H3K9m2 and H3K27m3 in wild-type and met1 plants, which we integrated with transcriptional data, to explore the relationships between these two marks. We found that ectopic H3K9m2 observed in met1 can be due to defects in IBM1-mediated H3K9m2 demethylation at some sites, but most importantly targets H3K27m3-marked genes, suggesting an interplay between these two silencing marks. Furthermore, H3K9m2/DNA-hypermethylation at these PcG targets in met1 is coupled with a decrease in H3K27m3 marks, whereas CG/H3K9m2 hypomethylated transposons become ectopically H3K27m3 hypermethylated. Our results bear interesting similarities with cancer cells, which show global losses of DNA methylation but ectopic hypermethylation of genes previously marked by H3K27m3. © 2012 Deleris et al.


Boulin T.,Institute Of Biologie Of Lecole Normale Superieure | Boulin T.,French Institute of Health and Medical Research | Boulin T.,French National Center for Scientific Research | Hobert O.,Columbia University
Wiley Interdisciplinary Reviews: Developmental Biology | Year: 2012

This review aims to provide an overview of the technologies which make the nematode Caenorhabditis elegans an attractive genetic model system. We describe transgenesis techniques and forward and reverse genetic approaches to isolate mutants and clone genes. In addition, we discuss the new possibilities offered by genome engineering strategies and next-generation genome analysis tools. © 2011 Wiley Periodicals, Inc.


Lickwar C.R.,Carolina Center for the Genome science | Mueller F.,Institute Of Biologie Of Lecole Normale Superieure | Mueller F.,Institute Pasteur Paris | Lieb J.D.,Carolina Center for the Genome science
Nature Protocols | Year: 2013

Competition chromatin immunoprecipitation (competition ChIP) enables experimenters to measure protein-DNA dynamics at a single locus or across the entire genome, depending on the detection method. Competition ChIP relies on a cell containing two copies of a single DNA-associated factor, with each copy of the factor differentially epitope tagged. One of the copies is expressed constitutively and the second is induced as a competitor. The ratio of isoforms associated with discrete genomic locations is detected by ChIP-on-chip (ChIP-chip) or ChIP-sequencing (ChIP-seq). The rate at which the resident isoform of the protein is replaced by the competitor at each binding location enables the calculation of residence time for that factor at each site of interaction genome wide. Here we provide a detailed protocol for designing and performing competition ChIP experiments in Saccharomyces cerevisiae, which takes ∼5 d to complete (not including strain production and characterizations, which may take as long as 6 months). Included in this protocol are guidelines for downstream bioinformatic analysis to extract residence times throughout the genome. © 2013 Nature America, Inc. All rights reserved.


Delgehyr N.,University of Cambridge | Delgehyr N.,Institute Of Biologie Of Lecole Normale Superieure | Rangone H.,University of Cambridge | Fu J.,University of Cambridge | And 5 more authors.
Current Biology | Year: 2012

Klp10A is a kinesin-13 of Drosophila melanogaster that depolymerizes cytoplasmic microtubules [1]. In interphase, it promotes microtubule catastrophe [2-4]; in mitosis, it contributes to anaphase chromosome movement by enabling tubulin flux [1, 5]. Here we show that Klp10A also acts as a microtubule depolymerase on centriolar microtubules to regulate centriole length. Thus, in both cultured cell lines and the testes, absence of Klp10A leads to longer centrioles that show incomplete 9-fold symmetry at their ends. These structures and associated pericentriolar material undergo fragmentation. We also show that in contrast to mammalian cells where depletion of CP110 leads to centriole elongation [6], in Drosophila cells it results in centriole length diminution that is overcome by codepletion of Klp10A to give longer centrioles than usual. We discuss how loss of centriole capping by CP110 might have different consequences for centriole length in mammalian [6-8] and insect cells and also relate these findings to the functional interactions between mammalian CP110 and another kinesin-13, Kif24, that in mammalian cells regulates cilium formation. © 2012 Elsevier Ltd.

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