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https://hdl.handle.net/123456789/787| Τύπος: | Αναρτημένη ανακοίνωση (poster) |
| Τίτλος: | Defects in actin and microtubule dynamics in mice missing Rac1 and Rac3 function |
| Συγγραφέας: | [EL] Κούνουπα, Ζουζάνα[EN] Kounoupa, Zouzana [EN] Tivodar, Simona [EL] Θεοδωράκης, Κώστας[EN] Theodorakis, Kostas [EL] Καραγωγέως, Δόμνα[EN] Karagogeos, Domna |
| 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 Biology [EL] Νευροεπιστήμες[EN] Neurosciences |
| Λέξεις-κλειδιά: | Rho GTPases; interneurons; migration |
| 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 |
| Εμφανίζεται στις συλλογές: | Ερευνητικές ομάδες |
Αρχεία σε αυτό το τεκμήριο:
| Αρχείο | Περιγραφή | Σελίδες | Μέγεθος | Μορφότυπος | Έκδοση | Άδεια | |
|---|---|---|---|---|---|---|---|
| poster 2018 (2) copy.pdf | 14.43 MB | Adobe PDF | - |  | Δείτε/ανοίξτε |