ArticleCell reports2026
SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
SNAREopathies are neurodevelopmental syndromes arising from de novo mutations in the synaptic machinery. Two variants are SNAP-25 I192N and I192T, which cause early lethality and moderate developmental delay, respectively. Both variants lead to destabilization of the C-terminal end of the SNARE complex and reduced binding to the Munc18-1:VAMP2:syntaxin-1 acceptor complex while reducing spontaneous and evoked synaptic release in autaptic glutamatergic neurons (severity: I192N > I192T). I192N, but not I192T, negatively affects neuronal survival and dendritic branching. I192N is strongly dominant negative in the presence of wild-type SNAP-25, leading to impaired survival and reduced synaptic release. The dominant-negative effect is stronger for spontaneous than for evoked release and mild for sustained release. We consider how release is affected upon random incorporation of variant and wild-type proteins into a ring of SNARE complexes. We suggest that only a subset (approximately three) of the pre-assembled SNAREs (approximately six) mediates evoked release, rendering evoked release less susceptible to variants.
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