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RIM3¿ and RIM4¿ are key regulators of neuronal arborization.

Authors: Alvarez-Baron, Elena  Michel, Katrin  Mittelstaedt, Tobias  Opitz, Thoralf  Schmitz, Frank  Beck, Heinz  Dietrich, Dirk  Becker, Albert J  Schoch, Susanne 
Citation: Alvarez-Baron E, etal., J Neurosci. 2013 Jan 9;33(2):824-39. doi: 10.1523/JNEUROSCI.2229-12.2013.
Pubmed: (View Article at PubMed) PMID:23303958
DOI: Full-text: DOI:10.1523/JNEUROSCI.2229-12.2013

The large isoforms of the Rab3 interacting molecule (RIM) family, RIM1α/ß and RIM2α/ß, have been shown to be centrally involved in mediating presynaptic active zone function. The RIM protein family contains two additional small isoforms, RIM3γ and RIM4γ, which are composed only of the RIM-specific C-terminal C2B domain and varying N-terminal sequences and whose function remains to be elucidated. Here, we report that both, RIM3γ and RIM4γ, play an essential role for the development of neuronal arborization and of dendritic spines independent of synaptic function. γ-RIM knock-down in rat primary neuronal cultures and in vivo resulted in a drastic reduction in the complexity of neuronal arborization, affecting both axonal and dendritic outgrowth, independent of the time point of γ-RIM downregulation during dendrite development. Rescue experiments revealed that the phenotype is caused by a function common to both γ-RIMs. These findings indicate that γ-RIMs are involved in cell biological functions distinct from the regulation of synaptic vesicle exocytosis and play a role in the molecular mechanisms controlling the establishment of dendritic complexity and axonal outgrowth.


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RGD Object Information
RGD ID: 13702404
Created: 2018-07-18
Species: All species
Last Modified: 2018-07-18
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.