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

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Cell Biology of the Neuron: Polarity, Plasticity and Regeneration, Crete 2011 Rassf1 and Rassf5 are required for Neuronal Polarity Rui Yang 1 , Eryan Kong 2 , Andreas W. Püschel 2 1 Institut für Molekulare Zellbiologie, Westfälische Wilhelms-Universität Münster, Germany and International Graduate Program Cell Dynamics and Disease (CEDAD) 2 Institut für Molekulare Zellbiologie, Westfälische Wilhelms-Universität Münster The polarized morphology of a neuron with a single axon and several dendrites is essential for its function in the directional flow of information in the central nervous system. Cultures of dissociated hippocampal neurons have proven invaluable to dissect the signaling pathways that direct the establishment of neuronal polarity. The early development of cultured neurons can be subdivided into 5 stages. Initially, neurons form several indistinguishable neurites, which all have the potential to become the axon (stage 1-2). In late stage 2, one of the neurites is specified as the axon and grows rapidly (stage 3) GTPases of the Ras family are central components of the signaling pathway that initiates axon extension. The Rassf (Ras-association domain family) proteins are a family of Ras effectors that are characterized by the shared Ras association domain and function as tumor suppressors. Through this domain, they interact with Ras GTPases, molecular switches that regulate a diverse range of cellular functions. In our study, we used cultured E18 rat hippocampal neurons to study the function of Rassf1 and Rassf5 in neuronal polarity. Neurons formed multiple axons when the expression of Rassf1 or Rassf5 was suppressed by RNAi. To address the question how Rassf1 and Rassf5 affect axon extension, we investigated the role of Ndr1 and Ndr2. Rassf1 interacts with MST (mammalian Sterile20-like 1) kinases, which in turn can activate the NDR (nuclear Dbf-2 related) kinases. The NDR kinases belong to the serine/threonine AGC (protein kinase A(PKA)/PKG/PKC-like) class of protein kinases that control important cellular processes, such as changes in cell morphology, mitotis, cytokinesis, and apoptosis. In neurons, NDR kinases have been implicated in mediating neurite tiling and regulating neurite growth. After knockdown of both NDR1 and NDR2, neurons formed multiple axons. Expression of NDR2 can rescue the knockdown phenotype of Rassf5, confirming that Rassf5 acts through NDR kinases. These experiments reveal a novel pathway that regulates neuronal polarity. Presented by: Yang, Rui Poster No 122 Green Session 204
Cell Biology of the Neuron: Polarity, Plasticity and Regeneration, Crete 2011 NMDA Receptor Activation Suppresses Microtubule Dynamics in Neurons Kah Wai Yau 1 , Lukas C. Kapitein 1 , Susana Montenegro Gouveia 2 , Wouter A. van der Zwan 1 , Phebe S. Wulf 1 , Jeroen Demmers 3 , Jacek Jaworski 4 , Anna Akhmanova 2 , Casper C. Hoogenraad 1 1 Department of Neuroscience, Erasmus Medical Center Rotterdam, The Netherlands 2 Department of Cell Biology, Erasmus Medical Center Rotterdam, The Netherlands 3 Proteomics Center, Erasmus Medical Center Rotterdam, The Netherlands 4 International Institute of Molecular and Cell Biology, Warsaw, Poland Dynamic microtubules are important to maintain neuronal morphology and function, but whether neuronal activity affects the organization of dynamic microtubules is unknown. Here we show that a protocol to induce NMDAdependent long-term depression (LTD) rapidly attenuates microtubule dynamics in primary hippocampal neurons, removing the microtubule binding protein EB3 from the growing microtubule plus-ends in dendrites. This effect requires the entry of calcium and is mediated by activation of NR2B-containing NMDA type glutamate receptor. The rapid NMDA effect is followed by a second, more prolonged response, during which EB3 accumulates along MAP2-positive microtubule bundles in the dendritic shaft. MAP2 is both required and sufficient for this activity-dependent redistribution of EB3. Importantly, NMDA receptor activation suppresses microtubule entry in dendritic spines, while overexpression of EB3-GFP prevents NMDA-induced spine shrinkage. Therefore, short-lasting and long-lasting changes in dendritic microtubule dynamics are important determinants for NMDA-induced LTD. Presented by: Yau, Kah Wai 205 Poster No 123 Blue Session
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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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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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