NeuroCoG Seminar Series: Monica Sousa, University of Porto, Portugal

on the September 27, 2019

11:00am to 1:00pm
From cytoskeleton to neuronal function
Organized by Frédéric Saudou
On September 27th, 2019, NeuroCoG invited Monica Sousa, Group Leader at IBMC/i3S, University of Porto, Annie Andrieux (GIN) and Isabelle Arnal (GIN) for a conference entitled "From cytoskeleton to neuronal function" at Grenoble Institut Neurosciences (GIN). Nearly 40 people attended these presentations on neural functioning that the practitioners wanted to be accessible, in the spirit of the cross disciplinary project Neurocog.
Program:

11am-12am: Monica Sousa - Regulation of axon diameter by the membrane periodic skeleton
12am-12.30pm: Annie Andrieux - Defective tubulin detyrosination causes structural brain abnormalities with cognitive deficiency in humans and mice.
12.30am-1pm: Isabelle Arnal - Cytoskeleton regulation by neuronal effectors:
New functions for old MAPs
1pm : Buffet
1.15pm - 2.15pm : Discussion between NeuroCoG PhD students and Monica Sousa
A time of exchanges between Monica Sousa and the doctoral and post-doctoral students recruited by NeuroCog, will be organized from 1:15pm to 2:15.


 

Monica Sousa - Group Leader - IBMC/i3S, UNiversity of Porto
Regulation of axon diameter by the membrane periodic skeleton

Abstract: After contacting their targets, axons increase their diameter to enable fast conduction of action potentials. In the adult, axonal caliber varies by almost 100-fold in different tracts. When considering a given axon, its diameter can further oscillate depending on organelle transport, neuronal activity, or deformations imposed by movement or degeneration. However, the fine-tune mechanisms controlling diameter throughout the lifetime of an axon, remain largely elusive. Here, we will present our most recent findings on the mechanisms regulating of axon diameter, with a specific focus on the role played by the actin-spectrin based membrane periodic skeleton, and their implications in neuronal biology.


Annie Andrieux, Group leader, Team "Physiopathologies of the Cytoskeleton"
Defective tubulin detyrosination causes structural brain abnormalities with cognitive deficiency in humans and mice.

Pierre Heemeryck, Alistair Pagnamenta, Hilary Martin, Christophe Bosc, Ivy Uszynski, Sylvie Gory-Faure, Frederique Vossier, Eric Denarier, Emmanuel Barbier, Jean-Christophe Deloulme, Jenny Taylor, Edward Blair, Annie Andrieux, and Marie-Jo Moutin.

Abstract: Reversible detyrosination of tubulin, the building block of microtubule, is crucial for neuron physiology. Enzymes in charge of detyrosination were recently identifed, by our team, as complexes of vasohibins 1 and 2 with small vasohibin-binding protein (SVBP). Here we report three consanguineous human families each containing multiple individuals with biallelic inactivation of SVBP, caused by two truncating variants. Affected individuals show brain abnormalities with microcephaly, intellectual disability and have delayed gross motor development. In the SVBP knockout mice brain, we observe a decrease of detyrosinated tubulin level and an increase of tyrosinated tubulin content. Morphological analysis of the SVBP knockout mouse brains by anatomical MRI showed a broad impact of SVBP loss, with a 7% brain volume decrease, numerous structural defects with more than 30% reduction of some white matter tracts. Behavioral tests shown that SVBP knockout mice are more active, less anxious, exhibit an impaired social behavior. Thus, SVBP KO mice recapitulate several deficiencies observed in human patient. Altogether, our data show that deleterious variants in SVBP, by causing major changes in brain tubulin tyrosination and alteration of microtubule dynamics, cause a neurodevelopmental pathology.

Isabelle Arnal - Group Leader - "Cytoskeleton dynamics and structure"
Cytoskeleton regulation by neuronal effectors: New functions for old MAPs

Abstract: Microtubules are major brain cytoskeletal components and are involved in neuronal development, morphology and functions. Neuronal microtubules can be highly dynamic or form stable arrays with various lifetimes; also they can be found as linear bundles along axons/dendrites or as single polymers like in synapses. Many effectors participate to the elaboration and plasticity of these diverse microtubule arrangements, yet the underlying mechanisms are still poorly understood. Microtubule-associated proteins (MAPs) are key actors of such regulation since they control microtubule assembly-disassembly, stability and self-organisation. Moreover, microtubules cooperate with actin, the other main neuronal cytoskeletal component, this interplay being crucial for neurite elongation and proper synapse functionality. I will present our recent work on two neuronal MAPs, tau and MAP6, which turn out not to be simply microtubule stabilizers but perform various other functions ranging from microtubule organisation and deformation to actin regulation and microtubule/actin coordination.










Published on October 1, 2019

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