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Journal Article

Seizure protein 6 controls glycosylation and trafficking of kainate receptor subunits GluK2 and GluK3

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Tran,  Mai Ly
von Blume, Julia / Molecular Basis of Protein Trafficking, Max Planck Institute of Biochemistry, Max Planck Society;

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von Blume,  Julia
von Blume, Julia / Molecular Basis of Protein Trafficking, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Pigoni, M., Hsia, H.-E., Hartmann, J., Rudan Njavro, J., Shmueli, M. D., Mueller, S. A., et al. (2020). Seizure protein 6 controls glycosylation and trafficking of kainate receptor subunits GluK2 and GluK3. EMBO JOURNAL, e103457. doi:10.15252/embj.2019103457.


Cite as: https://hdl.handle.net/21.11116/0000-0006-BA1E-8
Abstract
Seizure protein 6 (SEZ6) is required for the development and maintenance of the nervous system, is a major substrate of the protease BACE1 and is linked to Alzheimer's disease (AD) and psychiatric disorders, but its molecular functions are not well understood. Here, we demonstrate that SEZ6 controls glycosylation and cell surface localization of kainate receptors composed of GluK2/3 subunits. Loss of SEZ6 reduced surface levels of GluK2/3 in primary neurons and reduced kainate-evoked currents in CA1 pyramidal neurons in acute hippocampal slices. Mechanistically, loss of SEZ6in vitroandin vivoprevented modification of GluK2/3 with the human natural killer-1 (HNK-1) glycan, a modulator of GluK2/3 function. SEZ6 interacted with GluK2 through its ectodomain and promoted post-endoplasmic reticulum transport of GluK2 in the secretory pathway in heterologous cells and primary neurons. Taken together, SEZ6 acts as a new trafficking factor for GluK2/3. This novel function may help to better understand the role of SEZ6 in neurologic and psychiatric diseases.