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Séminaire Yasunori Hayashi

13 juillet 2018 / 11:30

The mechanism converting a transient Ca2+-signaling into persistent biochemical signaling during LTP., The mechanism converting a transient Ca2+-signaling into persistent biochemical signaling during LTP.

Abstract :

Long-term synaptic plasticity requires a mechanism that converts short Ca2+ pulses into persistent biochemical signaling to support the changes in the function and structure of synapses over long period of time. Here, we present a positive feedback loop, formed by a « reciprocally activating kinase-effector complex » (RAKEC) in dendritic spines, enabling the persistence and confinement of the molecular memory. We found that stimulation of a single spine causes the rapid formation of a RAKEC consists of a kinase CaMKII and its substrate a RacGEF TIAM1, which can stably promote actin-polymerization through Rac1, thereby maintaining the structure of the spine over a long period of time during LTP. This is achieved by a pseudo-autoinhibitory domain found within TIAM1, homologous to the autoinhibitory domain of CaMKII. RAKEC can store biochemical information in small subcellular compartments, thus potentially serving as a general mechanism for the production of prolonged and compartmentalized signaling.

Prochainement

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  2. Conférence Labex Trail – Goran Angelovski

    vendredi 28 juin 2019 / 14:30

    Molecular fMRI with Bioresponsive Probes

  3. Atout neurones

    samedi 29 juin 2019 / 14:00 - 20:00

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  4. Ramène (pas) ta science ! à la kermesse des sciences

    dimanche 30 juin 2019 / 14:00 - 23:00

    Parc Peixotto, Talence

  5. Séminaire – Anne Brunet

    mardi 2 juillet 2019 / 11:30

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Détails

Date :
13 juillet 2018
Heure :
11:30
Catégorie d’Évènement: