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Project 9

Ubiquitylation-controlled Arc/Arg3.1 translation and protein turnover in synaptic plasticity and memory consolidation

Enduring forms of synaptic plasticity and long-term memory are dependent on gene transcription and protein synthesis. A specific example can be seen in the expression of Arc/Arg3.1 which is essential for the consolidation of synaptic plasticity and memories. Upon plasticity-producing stimulation Arc/Arg3.1 mRNA is induced and targeted to dendrites. Within dendrites Zinki, an mRNA binding protein that acts as a repressor of Arc/Arg3.1 translation, becomes degraded via the ubiquitin/proteasome system. Besides activity-dependent relief of translational repression, Arc/Arg3.1 protein has a short halflife, suggesting additional regulation of Arc/Arg3.1 by protein turnover. We will ask the following questions: i) how translational control of Arc/Arg3.1 mRNA is exerted by the dendritic mRNA binding protein Zinki, ii) determine how activity-dependent ubiquitylation and proteasomal degradation of Zinki might contribute to synaptic input specificity, iii) define the molecular pathways that control Arc/Arg3.1 protein turnover and iv) ask what functional consequence these bear on AMPA receptor trafficking, homeostasis, plasticity, and memory.

Adress:

Prof. Dr. Dietmar Kuhl
Institute of Molecular and Cellular Cognition (IMCC)
Center for Molecular Neurobiology (ZMNH)
University Medical Center Hamburg-Eppendorf (UKE)
Falkenried 94
D-20251 Hamburg
Tel.: +49 40 7410 56277
FAX: +49 40 7410 55101
E-Mail: kuhl@zmnh.uni-hamburg.de

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last update: Dieter Münch-Harrach, 11.11.2010