The synaptic vesicle protein 2C mediates the uptake of botulinum neurotoxin A into phrenic nerves | Zendy

Mahrhold Stefan | Zendy; Rummel Andreas | Zendy; Bigalke Hans | Zendy; Davletov Bazbek | Zendy; Binz Thomas | Zendy

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The synaptic vesicle protein 2C mediates the uptake of botulinum neurotoxin A into phrenic nerves

Author(s) -

Mahrhold Stefan,

Rummel Andreas,

Bigalke Hans,

Davletov Bazbek,

Binz Thomas

Publication year - 2006

Publication title -

febs letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.593

H-Index - 257

eISSN - 1873-3468

pISSN - 0014-5793

DOI - 10.1016/j.febslet.2006.02.074

Subject(s) - synaptotagmin 1 , synaptic vesicle , snap25 , vesicle fusion , chemistry , microbiology and biotechnology , transmembrane domain , transmembrane protein , vesicle , kiss and run fusion , phrenic nerve , neurotoxin , neurotransmitter , biochemistry , biology , biophysics , receptor , membrane , anatomy , respiratory system

Botulinum neurotoxins (BoNTs) inhibit neurotransmitter release by selectively cleaving core components of the vesicular fusion machinery. The synaptic vesicle proteins Synaptotagmin‐I and ‐II act as receptors for BoNT/B and BoNT/G. Here we show that BoNT/A also interacts with a synaptic vesicle protein, the synaptic vesicle glycoprotein 2C (SV2C), but not with the homologous proteins SV2A and SV2B. Binding of BoNT/A occurs at the membrane juxtaposed region preceding transmembrane domain 8. A peptide comprising the intravesicular domain between transmembrane domains 7 and 8 specifically reduces the neurotoxicity of BoNT/A at phrenic nerve preparations demonstrating the physiological relevance of this interaction.

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