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• W2332932623 abstract "Event Abstract Back to Event The absence of Rac1 and Rac3 significantly affects actin-microtubule dynamics in developing cortical interneurons. Simona Tivodar1, Katerina Kalemaki1*, Zouzana Kounoupa1, Marina Vidaki2, Kostas Theodorakis1, Myrto Denaxa3, Nicoletta Kessaris4, Ivan De Curtis5, Vassilis Pachnis3 and Domna Karagogeos1* 1 Institute of Molecular Biology and Biotechnology (IMBB),FORTH, Neurosciences Division, Greece 2 Koch Institute for Integrative Cancer Research at MIT, Massachusetts Institute of Technology, United States 3 Division of Molecular Neurobiology, Medical Research Council, National Institute for Medical Research, United Kingdom 4 Wolfson Institute for Biomedical Research and Department of Cell & Developmental Biology, University College London, United Kingdom 5 Cell Adhesion Unit, Dibit, San Raffaele Scientific Institute, Italy The proper function of the CNS requires the correct integration of glutamatergic neurons and GABAergic interneurons. Cortical GABAergic interneurons are characterized by extraordinary neurochemical and functional diversity. Although recent studies have uncovered some of the molecular components underlying interneuron development, including the cellular and molecular mechanisms guiding their migration to the cortex, the intracellular components involved in these processes are still unknown. Rac-proteins are RhoGTPases that integrate multiple extracellular signals required for essential processes in diverse cell types as cytoskeleton organization, vesicle trafficking, transcription, cell cycle progression, and apoptosis. We examined the role of the ubiquitous Rac1 and neural-specific Rac3 in interneurons derived from the medial ganglionic eminence (MGE). Previously we used Cre/loxP technology to uncover a cell autonomous and stage-specific requirement for Rac1 activity within proliferating interneurons. Most Rac1 conditional mutant mice die after 3-6 weeks due to epileptic seizures as a result of the presence of 50% of GABAergic interneurons postnatally. In addition, Rac1 mutant MGE cells in vitro show cytoskeletal alterations in growth cone formation and a significant reduction of the leading process length (Vidaki et al., 2012). However, the simultaneous absence of Rac1 and Rac3 results not only in additive but also distinctive defects. Double mutant mice die earlier and display a dramatic (80%) loss of cortical interneurons, evident from embryonic stages. In addition to the Rac1 specific defects, Rac1/Rac3-deficient interneurons show gross cytoskeletal defects in vitro, with a prominent polarity-related defect (Tivodar et al., 2014). Stabilization of mictrotubules improves neuronal growth and polarity. We propose that in the absence of Rac1/Rac3 cortical interneurons fail to tangentially migrate towards the pallium due to defects in actin-microtubule cytoskeletal dynamics that we are currently analyzing. Keywords: Cortical development, Cytoskeleton, medial ganglionic eminence, Rho-GTPases, GABAergic interneurons Conference: 4th NAMASEN Training Workshop - Dendrites 2014, Heraklion, Greece, 1 Jul - 4 Jul, 2014. Presentation Type: Poster presentation Topic: morphological and functional characterizations Citation: Tivodar S, Kalemaki K, Kounoupa Z, Vidaki M, Theodorakis K, Denaxa M, Kessaris N, De Curtis I, Pachnis V and Karagogeos D (2014). The absence of Rac1 and Rac3 significantly affects actin-microtubule dynamics in developing cortical interneurons.. Front. Syst. Neurosci. Conference Abstract: 4th NAMASEN Training Workshop - Dendrites 2014. doi: 10.3389/conf.fnsys.2014.05.00001 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 01 Jun 2014; Published Online: 12 Jun 2014. * Correspondence: Ms. Katerina Kalemaki, Institute of Molecular Biology and Biotechnology (IMBB),FORTH, Neurosciences Division, Heraklion, Greece, kalemaki@imbb.forth.gr Prof. Domna Karagogeos, Institute of Molecular Biology and Biotechnology (IMBB),FORTH, Neurosciences Division, Heraklion, Greece, karagoge@imbb.forth.gr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Simona Tivodar Katerina Kalemaki Zouzana Kounoupa Marina Vidaki Kostas Theodorakis Myrto Denaxa Nicoletta Kessaris Ivan De Curtis Vassilis Pachnis Domna Karagogeos Google Simona Tivodar Katerina Kalemaki Zouzana Kounoupa Marina Vidaki Kostas Theodorakis Myrto Denaxa Nicoletta Kessaris Ivan De Curtis Vassilis Pachnis Domna Karagogeos Google Scholar Simona Tivodar Katerina Kalemaki Zouzana Kounoupa Marina Vidaki Kostas Theodorakis Myrto Denaxa Nicoletta Kessaris Ivan De Curtis Vassilis Pachnis Domna Karagogeos PubMed Simona Tivodar Katerina Kalemaki Zouzana Kounoupa Marina Vidaki Kostas Theodorakis Myrto Denaxa Nicoletta Kessaris Ivan De Curtis Vassilis Pachnis Domna Karagogeos Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page." @default.
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• W2332932623 title "The absence of Rac1 and Rac3 significantly affects actin-microtubule dynamics in developing cortical interneurons." @default.
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