Protein SUMOylation modulates calcium influx and glutamate release from presynaptic terminals

European Journal of Neuroscience - Tập 29 Số 7 - Trang 1348-1356 - 2009
Marco Feligioni1, Atsushi Nishimune2, Jeremy M. Henley3
1Department of Anatomy, MRC Centre for Synaptic Plasticity, School of Medical Sciences, University of Bristol, Bristol, UK
2MRC Centre for Synaptic Plasticity, Department of Anatomy, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK
3Bristol Neuroscience

Tóm tắt

AbstractPosttranslational modification by small ubiquitin‐like modifier (SUMO) proteins is emerging as an important regulatory mechanism for neuronal function and dysfunction. Although multiple potential presynaptic SUMOylation substrate proteins have been proposed from sequence analysis the functional consequences of presynaptic SUMOylation have not been determined. Here we show that SUMOylation of presynaptic proteins modulates neurotransmitter release. Increasing protein SUMOylation by entrapping recombinant SUMO‐1 in synaptosomes decreased glutamate release evoked by KCl whereas decreasing SUMOylation with the SUMO‐specific protease SENP‐1 enhanced KCl‐evoked release. In contrast, SUMO increased and SENP‐1 decreased synaptosomal glutamate release evoked by kainate stimulation. Consistent with these results, SENP‐1 increased Ca2+ influx into synaptosomes evoked by KCl whereas it decreased kainate‐induced Ca2+ influx. These results demonstrate that, in addition to postsynaptic effects, protein SUMOylation acts to modulate neurotransmitter release and thereby regulate synaptic function.

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European Journal of Neuroscience

Tập 29 Số 7

1348-1356

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