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Neuron. 2014 Sep 3;83(5):1051-7. doi: 10.1016/j.neuron.2014.07.043. Epub 2014 Aug 21.

Efficient, complete deletion of synaptic proteins using CRISPR.

Author information

1
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA.
2
Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
3
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: roger.nicoll@ucsf.edu.

Erratum in

  • Neuron. 2015 Nov 4;88(3):617.

Abstract

One of the most powerful ways to test the function of a protein is to characterize the consequences of its deletion. In the past, this has involved inactivation of the gene by homologous recombination either in the germline or later through conditional deletion. RNA interference (RNAi) provides an alternative way to knock down proteins, but both of these approaches have their limitations. Recently, the CRISPR/Cas9 system has suggested another way to selectively inactivate genes. We have now tested this system in postmitotic neurons by targeting two well-characterized synaptic proteins, the obligatory GluN1 subunit of the NMDA receptor and the GluA2 subunit of the AMPA receptor. Expression of CRISPR/Cas9 in hippocampal slice cultures completely eliminated NMDA receptor and GluA2 function. CRISPR/Cas9 thus provides a powerful tool to study the function of synaptic proteins.

PMID:
25155957
PMCID:
PMC4195490
DOI:
10.1016/j.neuron.2014.07.043
[Indexed for MEDLINE]
Free PMC Article

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