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

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Cell Biology of the Neuron: Polarity, Plasticity and Regeneration, Crete 2011 Tubulin Polyglutamylation: a Role in Neuronal Polarity and Transport Maria Magiera, Judith Souphron, Diana Zala, Frederic Saudou, Carsten Janke Institut Curie Neurons are polarized cells and their cell body, dendrites and axon differ radically in terms of morphology, function and molecular composition. The specification of the axonal and dendritic identity occurs early in neuronal development and is maintained for decades. The mechanisms of neuron polarity establishment, maintenance and loss are not fully understood, but microtubules (MTs) seem to play an important role in these processes. Many MT-associated proteins (MAPs) and motors can be found exclusively in one of the cellular compartments, and strikingly, this distribution can be perturbed in degenerating neurons. Neuronal MTs are heavily polyglutamylated, and we have shown that deregulation of the levels of this posttranslational modification of tubulin leads to neurodegeneration. We are now interested by which mechanism tubulin polyglutamylation controls neuronal survival and we want to investigate whether it could influence the establishment and maintenance of neuronal polarity. Using primary cultures of mouse hippocampal neurons we modulate tubulin glutamylation and study the consequences of these changes on cell morphology, MAP distribution, motor traffic, axon branching, growth cone function and possible degenerative processes. First experiments have shown that tubulin is differentially modified in axons vs. dendrites and that changing tubulin glutamylation pattern in developing neurons can influence MAP localization. We are now establishing an assay allowing quantifying the impact of polyglutamylation levels on axonal transport parameters. In the next step we will investigate the role of MT polyglutamylation on MAP and motor binding and behaviour in cell-free in vitro systems. Presented by: Magiera, Maria Poster No 068 Green Session 150
Cell Biology of the Neuron: Polarity, Plasticity and Regeneration, Crete 2011 Identifying Injury Signals and Regeneration Enhancers in the Conditioning Lesion Model Fernando Mar 1 , Marques Ana 1 , Brites Pedro 1 , António Barbosa 2 , Vitor Costa 2 1 , Mónica Sousa 1 IBMC - Nerve Regeneration group 2 IBMC - cellular and applied microbiology Following PNS lesion, injury is signaled by retrograde transport of positive injury signals, such as p-ERK, which lead to transcription of regeneration enhancers anterogradely transported to the injury site. These changes induced by a PNS lesion are thought to enable DRG neurons to regenerate central branch axons following a subsequent spinal cord injury (SCI) - conditioning lesion effect. However, the identity of the newly synthesized enhancers remains unclear. To assess if the inability of central DRG axons to regenerate is at least partially due to lack of synthesis and transport of injury signals to the DRG, dorsal root crush was performed and transport of known injury signals was tested. Following dynein immunoprecipitation, an increase in p-ERK was detected in the injured dorsal root similarly to what is seen after sciatic nerve injury (SNI). This suggests that transport of injury signals following a lesion to the DRG central branch occurs. However it argues against the role of p-ERK in mounting a regenerative response since after a dorsal root crush, DRG neurons do not present increased neurite outgrowth as observed following SNI. To identify regeneration enhancers synthesized in the DRG and anterogradely transported to the SCI site following a conditioning injury, these were radiolabeled, tracked and compared in animals following SCI or conditioning lesion. We found an increase in radiolabeled proteins transported to the spinal cord of animals with a conditioning injury. This increase was mainly due to higher synthesis of cytoskeleton-related and glycolitic proteins although the synthesis and transport of putative novel regeneration enhancers, including RhoGDI-1 and CRMP-5, was also detected. Future work will concentrate on clarifying the role of described injury signals in the regenerative process and on determining the relevance for axonal growth of the putative novel regeneration enhancers identified. Presented by: Mar, Fernando 151 Poster No 069 Blue Session
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Abstracts of papers presented at th
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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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Cell Biology of the Neuron: Polarit
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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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