CELL BIOLOGY OF THE NEURON Polarity ... - Tavernarakis Lab

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Cell Biology of the Neuron: <strong>Polarity</strong>, Plasticity and Regeneration, Crete 2011 Activity-Driven AMPA Receptor Remodelling in Hippocampus Mediated by RNA Editing Ales Balik 1 , Andrew Penn, Christian Wozny, Ingo Greger 1 MRC-LMB, Cambridge, UK Signalling at excitatory synapses is determined by the composition of the AMPAR complex, which differs during development and depends upon the history of synaptic excitation. The rules controlling AMPAR assembly in the endoplasmic reticulum are not well established. Alternative splicing (flip/flop exons) and RNA editing (R/G site) in the ligand-binding domain (LBD) are implicated in subunit assembly of recombinant AMPARs. Both alternative processed sites strategically located on the interface of LBD modulate receptor tetramer. Here we reveal a dynamic RNA reprogramming at these sites in response to altered neuronal activity within hippocampus. RNA processing is bidirectional depending on the sign of activity and selectively occurs in the CA1 subfield. Observed global changes in RNA processing have been also detected at the level of individual pyramidal neurons. Level of R/G site editing evidently correlates with expression and self-editing of the editase enzyme ADAR2. Using different electrophysiology approaches we found altered functional properties of AMPARs in activity deprived cells. The subunit composition of surfaceexpressed AMPARs was unchanged. However, high-resolution recordings indicate that changes observed at the level of recoded mRNA (proportion of edited/unedited flip form) have the capacity to translate into remodelled AMPARs. We integrate our findings into an assembly model that could account for the differences between AMPAR splice variant expression and the pharmacological and functional properties of synapticaly-expressed receptors. Our results suggest that RNA editing provides a dynamic mechanism capable of adjusting response properties in neuronal circuits by AMPAR subunit remodelling. Presented by: Balik, Ales Poster No 002 Green Session 84
Cell Biology of the Neuron: <strong>Polarity</strong>, Plasticity and Regeneration, Crete 2011 The Function of the Zinc-Finger Factor Insm1 in Postnatal Neurogenesis Kira Balueva 1 , Camille Boutin 2 , Harold Cremer 2 , Carmen Birchmeier 1 1 Max-Delbrueck-Centrum for Molecular Medicine, MDC 2 Developmental Biology Institute of Marseille-Luminy, IBDML The Insulinoma-associated 1 (Insm1) gene encodes a putative transcription factor. Insm1 is expressed in neuroendocrine tumors, in developing and adult endocrine cells, and in the nervous system. Interestingly, Insm1 is expressed transiently during differentiation of all neuronal cell types. In the postnatal and adult nervous system, Insm1 expression is restricted to neurogenic regions in the forebrain. Expression is detected in the subventricular zone of the lateral ventricles, in the rostral migratory stream and the dentate gyrus of the hippocampus. To define the role of Insm1 in adult neurogenesis, we used Cre-mediated conditional recombination of Insm1Floxed allele to ablate Insm1 expression in the subventricular zone of the forebrain. Cre was either expressed using transgenic technology i.e. the Brn4Cre allele, or it was delivered by electroporation. We found that the lack of Insm1 cell-autonomously affected development of neuronal progenitors in the postnatal olfactory system. In particular, mutation of Insm1 caused prolonged expression of Mash1, and delayed neuronal differentiation: neuronal migration was slower, and the numbers of mature granule neurons of the olfactory bulb generated within a defined time window were reduced. Thus, the lack of Insm1 interfered with neuronal differentiation. However, it did not block differentiation completely. The delay in differentiation was accompanied by an increase in the numbers of neuronal progenitors and neuroblasts in the subventricular zone and the rostral migratory stream of Insm1 mutant mice. Our data indicate that Insm1 is essential for the exit from the amplifying progenitor state, and that its mutation leads to prolonged replication of postnatal neuronal progenitors. Presented by: Balueva, Kira 85 Poster No 003 Blue Session
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The meeting was funded in part by E
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These abstracts should not be cited
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CYFIP1, a Neuronal eIF4E‐BP, Link
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POSTER ABSTRACTS Poster # [‐R(ed)
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030‐B Paracrine Pax6 Activity Reg
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058‐R Dynein Light Chain LC8 is a
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088‐R Spectraplakins ‐ Cytoskel
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121‐R Calmyrin1 Binds to SCG10 Pr
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18.00 ‐ 18.15 Non Hyperpolarizing
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10.00 ‐ 10.30 Neurotrophin Regula
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SESSION 10 SYNAPTOGENESIS Chairpers
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da F. Costa, L. 119 D'Adamo, P. 108
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Lewallen, K. 145 Li, Y.‐H. 201 Li
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Teuling, E. 141 Thiebes, K. 87 Thom
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Dr. Christian Alfano INSERM U636, N
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Prof. Graeme W. Davis University of
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Prof. Zhigang He Harvard Medical Sc
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Dr. Bernhard Lohkamp Karolinska Ins
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Mr. Abhishek Shrikant Sahasrabudhe
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Dr. Med. Andreas Vlachos Goethe‐U
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