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Τύπος: Αναρτημένη ανακοίνωση (poster)
Τίτλος: Defects in actin and microtubule dynamics in mice missing Rac1 and Rac3 function
Συγγραφέας: [EL] Κούνουπα, Ζουζάνα[EN] Kounoupa, Zouzanasemantics logo
[EN] Tivodar, Simonasemantics logo
[EL] Θεοδωράκης, Κώστας[EN] Theodorakis, Kostassemantics logo
[EL] Καραγωγέως, Δόμνα[EN] Karagogeos, Domnasemantics logo
Ημερομηνία: Σεπ-2018
Περίληψη: The correct function of cortical microcircuits depends in part on GABAergic interneurons that provide the main source of inhibition. Impaired interneuronal function results in severe neurodevelopmental disorders such as schizophrenia, epilepsy and autism. Interneuron migration from their origin to the neocortex is a pivotal process and is determined by extracellular factors which modify their leading processes through activation of intracellular pathways. Rac-proteins are intracellular mediators of numerous developmental processes such as cytoskeleton organization, vesicle trafficking, transcription, cell cycle progression in diverse cell types. We focus in the role of the ubiquitous Rac1 and neural-specific Rac3 in interneurons derived from the medial ganglionic eminence (MGE), a population comprising the majority of cortical interneurons. We previously uncovered, using Cre/loxP technology, a cell autonomous and stage-specific requirement for Rac1 activity within proliferating interneuron precursors (Vidaki et al, 2012). We have also generated Rac1/Rac3 double mutant mice (Tivodar et al, 2014) and found that in the absence of both Racs, the embryonic migration of MGE-derived interneurons is impaired, resulting in an 80% loss of cortical interneurons, postnatally. Rac1/Rac3-deficient interneurons show gross cytoskeletal defects when grown in vitro, including nuclear shape alterations, reduction of axon length, splitting of the leading process, abnormal growth cone formation and reduction of microtubule stability. Currently, we are investigating their migratory behavior using ex vivo time-lapse imaging; a number of motility parameters such as velocity, amplitude and frequency of nuclear translocation are decreased significantly. There is also a delay in principal neurite outgrowth. Our data indicate that in the absence of Rac1/Rac3, cortical interneurons fail to migrate to the cortex due to defects in actin and microtubule cytoskeletal dynamics.
Γλώσσα: Αγγλικά
Τόπος δημοσίευσης: Prague, Czech Republic
Σελίδες: 1
Θεματική κατηγορία: [EL] Αναπτυξιακή βιολογία[EN] Developmental Biologysemantics logo
[EL] Νευροεπιστήμες[EN] Neurosciencessemantics logo
Λέξεις-κλειδιά: Rho GTPasesinterneuronsmigration
Κάτοχος πνευματικών δικαιωμάτων: © by the author(s)
Σελίδες τεκμηρίου (στην πηγή): 1
Όνομα εκδήλωσης: FEBS Advance Lecture Course and 33rd European Cytoskeletal Forum Meeting
Τοποθεσία εκδήλωσης: Prague, Czech Republic
Ημ/νία έναρξης εκδήλωσης: 20/09/2018
Ημ/νία λήξης εκδήλωσης: 24/09/2018
Σημειώσεις: More information – https://cytoskeleton2018.febsevents.org.
Funding: Manasaki scholarship and ΕΔΜ34/ΚΑ10040, ΕΣΠΑ
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