Emilie PACARY




Chercheur

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Cursus:
- 2020, HDR , University of Bordeaux
-January 2007 to June 2012, Postdoc in François Guillemot’s lab, National Institute for Medical Research (London, UK)
- 2006, Ph.D. 'Biology, Medicine and Health', option Neurosciences; University of Caen, UMR CNRS 6185, Centre CYCERON (France)


Expertise: neurogenesis, RhoGTPases, neuronal development, Rnd proteins





29 publication(s) depuis Février 2005:


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* equal contribution
Les IF indiqués ont été collectés par le Web of Sciences en


19/03/2021 | Nat Commun   IF 12.1
Adult-born neurons immature during learning are necessary for remote memory reconsolidation in rats.
Lods M, Pacary E, Mazier W, Farrugia F, Mortessagne P, Masachs N, Charrier V, Massa F, Cota D, Ferreira G, Abrous DN, Tronel S

Abstract:
Memory reconsolidation, the process by which memories are again stabilized after being reactivated, has strengthened the idea that memory stabilization is a highly plastic process. To date, the molecular and cellular bases of reconsolidation have been extensively investigated particularly within the hippocampus. However, the role of adult neurogenesis in memory reconsolidation is unclear. Here, we combined functional imaging, retroviral and chemogenetic approaches in rats to tag and manipulate different populations of rat adult-born neurons. We find that both mature and immature adult-born neurons are activated by remote memory retrieval. However, only specific silencing of the adult-born neurons immature during learning impairs remote memory retrieval-induced reconsolidation. Hence, our findings show that adult-born neurons immature during learning are required for the maintenance and update of remote memory reconsolidation.




15/10/2020 | Small GTPases
Pathophysiological functions of Rnd proteins.
Basbous S, Azzarelli R, Pacary E, Moreau V

Abstract:
Rnd proteins constitute a subfamily of Rho GTPases represented in mammals by Rnd1, Rnd2 and Rnd3. Despite their GTPase structure, their specific feature is the inability to hydrolyse GTP-bound nucleotide. This aspect makes them atypical among Rho GTPases. Rnds are regulated for their expression at the transcriptional or post-transcriptional levels and they are activated through post-translational modifications and interactions with other proteins. Rnd proteins are mainly involved in the regulation of the actin cytoskeleton and cell proliferation. Whereas Rnd3 is ubiquitously expressed, Rnd1 and 2 are tissue-specific. Increasing data has described their important role during development and diseases. Herein, we describe their involvement in physiological and pathological conditions with a focus on the neuronal and vascular systems, and summarize their implications in tumorigenesis.




15/10/2020 | Small GTPases
Pathophysiological functions of Rnd proteins
Basbous S, Azzarelli R, Pacary E, Moreau V

Abstract:





Abstract:
The calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous and central player in Ca(2+) signaling that is best known for its functions in the brain. In particular, the ? isoform of CaMKII has been the subject of intense research and it has been established as a central regulator of neuronal plasticity. In contrast, little attention has been paid to CaMKII?, the other predominant brain isoform that interacts directly with the actin cytoskeleton, and the functions of CaMKII? in this organ remain largely unexplored. However, recently, the perturbation of CaMKII? expression has been associated with multiple neuropsychiatric and neurodevelopmental diseases, highlighting CAMK2B as a gene of interest. Herein, after highlighting the main structural and expression differences between the ? and ? isoforms, we will review the specific functions of CaMKII?, as described so far, in neuronal development and plasticity, as well as its potential implication in brain diseases.




10/09/2020 | BioRxiv
The atypical Rho GTPase Rnd2 is critical for dentate granule neuron development and anxiety-like behavior during adult but not neonatal neurogenesis
Kerloch T, Farrugia F, Maitre M, Terral G, Koehl M, Heng JI, Blanchard M, Doat H, Leste-Lasserre T, Goron A, Gonzales D, Guillemot F, Abrous DN, Pacary E

Abstract:





11/2018 | Mol Psychiatry   IF 11.6
A novel role for CAMKIIbeta in the regulation of cortical neuron migration: implications for neurodevelopmental disorders.
Nicole O, Bell DM, Leste-Lasserre T, Doat H, Guillemot F, Pacary E

Abstract:
Perturbation of CaMKIIbeta expression has been associated with multiple neuropsychiatric diseases, highlighting CaMKIIbeta as a gene of interest. Yet, in contrast to CaMKIIalpha, the specific functions of CaMKIIbeta in the brain remain poorly explored. Here, we reveal a novel function for this CaMKII isoform in vivo during neuronal development. By using in utero electroporation, we show that CaMKIIbeta is an important regulator of radial migration of projection neurons during cerebral cortex development. Knockdown of CaMKIIbeta causes accelerated migration of nascent pyramidal neurons, whereas overexpression of CaMKIIbeta inhibits migration, demonstrating that precise regulation of CaMKIIbeta expression is required for correct neuronal migration. More precisely, CaMKIIbeta controls the multipolar-bipolar transition in the intermediate zone and locomotion in the cortical plate through its actin-binding and -bundling activities. In addition, our data indicate that a fine-tuned balance between CaMKIIbeta and cofilin activities is necessary to ensure proper migration of cortical neurons. Thus, our findings define a novel isoform-specific function for CaMKIIbeta, demonstrating that CaMKIIbeta has a major biological function in the developing brain.




11/2018 | Mol Psychiatry   IF 11.6
CaMKIIbeta regulates nucleus-centrosome coupling in locomoting neurons of the developing cerebral cortex.
Nicole O, Bell DM, Leste-Lasserre T, Doat H, Guillemot F, Pacary E

Abstract:





Abstract:
In nonhuman mammals and in particular in rodents, most granule neurons of the dentate gyrus (DG) are generated during development and yet little is known about their properties compared with adult-born neurons. Although it is generally admitted that these populations are morphologically indistinguishable once mature, a detailed analysis of developmentally born neurons is lacking. Here, we used in vivo electroporation to label dentate granule cells (DGCs) generated in mouse embryos (E14.5) or in neonates (P0) and followed their morphological development up to 6 months after birth. By comparison with mature retrovirus-labeled DGCs born at weaning (P21) or young adult (P84) stages, we provide the evidence that perinatally born neurons, especially embryonically born cells, are morphologically distinct from later-born neurons and are thus easily distinguishable. In addition, our data indicate that semilunar and hilar GCs, 2 populations in ectopic location, are generated during the embryonic and the neonatal periods, respectively. Thus, our findings provide new insights into the development of the different populations of GCs in the DG and open new questions regarding their function in the brain.




06/07/2017 | eLife   IF 7.7
Physiological and pathophysiological control of synaptic GluN2B-NMDA receptors by the C-terminal domain of amyloid precursor protein.
Pousinha PA, Mouska X, Raymond EF, Gwizdek C, Dhib G, Poupon-Silvestre G, Zaragosi LE, Giudici C, Bethus I, Pacary E, Willem M, Marie H

Abstract:
The amyloid precursor protein (APP) harbors physiological roles at synapses and is central to Alzheimer's disease (AD) pathogenesis. Evidence suggests that APP intracellular domain (AICD) could regulate synapse function, but the underlying molecular mechanisms remain unknown. We addressed AICD actions at synapses, per se, combining in-vivo AICD expression, ex-vivo AICD delivery or APP knock-down by in utero electroporation of shRNAs with whole-cell electrophysiology. We report a critical physiological role of AICD in controlling GluN2B-containing NMDA receptors (NMDARs) at immature excitatory synapses, via a transcription-dependent mechanism. We further show that AICD increase in mature neurons, as reported in AD, alters synaptic NMDAR composition to an immature-like GluN2B-rich profile. This disrupts synaptic signal integration, via over-activation of SK channels, and synapse plasticity, phenotypes rescued by GluN2B antagonism. We provide a new physiological role for AICD, which becomes pathological upon AICD increase in mature neurons. Thus, AICD could contribute to AD synaptic failure.




03/10/2016 | curr protoc neurosci
Cerebral Cortex Electroporation to Study Projection Neuron Migration.
Pacary E, Guillemot F

Abstract:
Brain electroporation is a rapid and powerful approach to study neuronal development. In particular, this technique has become a method of choice for studying the process of radial migration of projection neurons in the embryonic cerebral cortex. This method has considerably helped to describe in detail the different steps of radial migration and to characterize the molecular mechanisms controlling this process. Delineating the complexities of neuronal migration is critical to our understanding not only of normal cerebral cortex formation but also of neurodevelopmental disorders resulting from neuronal migration defects. Here, we describe in detail the protocols to perform in utero or ex vivo electroporation of progenitor cells in the ventricular zone of the cerebral cortex with the aim of studying the process of radial migration of projection neurons during embryonic development. (c) 2016 by John Wiley & Sons, Inc.