학술논문

SNAP-25, but not SNAP-23, is essential for photoreceptor development, survival, and function in mice.
Document Type
Article
Source
Communications Biology. 1/5/2024, Vol. 7 Issue 1, p1-14. 14p.
Subject
*PHOTORECEPTORS
*SYNAPTIC vesicles
*KNOCKOUT mice
*PHOTOSYNTHETIC pigments
*GENE expression
Language
ISSN
2399-3642
Abstract
SNARE-mediated vesicular transport is thought to play roles in photoreceptor glutamate exocytosis and photopigment delivery. However, the functions of Synaptosomal-associated protein (SNAP) isoforms in photoreceptors are unknown. Here, we revisit the expression of SNAP-23 and SNAP-25 and generate photoreceptor-specific knockout mice to investigate their roles. Although we find that SNAP-23 shows weak mRNA expression in photoreceptors, SNAP-23 removal does not affect retinal morphology or vision. SNAP-25 mRNA is developmentally regulated and undergoes mRNA trafficking to photoreceptor inner segments at postnatal day 9 (P9). SNAP-25 knockout photoreceptors develop normally until P9 but degenerate by P14 resulting in severe retinal thinning. Photoreceptor loss in SNAP-25 knockout mice is associated with abolished electroretinograms and vision loss. We find mistrafficked photopigments, enlarged synaptic vesicles, and abnormal synaptic ribbons which potentially underlie photoreceptor degeneration. Our results conclude that SNAP-25, but not SNAP-23, mediates photopigment delivery and synaptic functioning required for photoreceptor development, survival, and function. A study using photoreceptor-specific knockout mice finds that SNAP-25, and not SNAP-23, is the isoform crucial for photoreceptor development, survival, and function. Mechanistically, SNAP-25 mediates photopigment trafficking and synaptic functioning. [ABSTRACT FROM AUTHOR]