| First Author | Yao J | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 7 | Pages | e68215 |
| PubMed ID | 23894296 | Mgi Jnum | J:204383 |
| Mgi Id | MGI:5532434 | Doi | 10.1371/journal.pone.0068215 |
| Citation | Yao J, et al. (2013) Loss of the SV2-like protein SVOP produces no apparent deficits in laboratory mice. PLoS One 8(7):e68215 |
| abstractText | Neurons express two families of transporter-like proteins - Synaptic Vesicle protein 2 (SV2A, B, and C) and SV2-related proteins (SVOP and SVOPL). Both families share structural similarity with the Major Facilitator (MF) family of transporters. SV2 is present in all neurons and endocrine cells, consistent with it playing a key role in regulated exocytosis. Like SV2, SVOP is expressed in all brain regions, with highest levels in cerebellum, hindbrain and pineal gland. Furthermore, SVOP is expressed earlier in development than SV2 and is one of the neuronal proteins whose expression declines most during aging. Although SV2 is essential for survival, it is not required for development. Because significant levels of neurotransmission remain in the absence of SV2 it has been proposed that SVOP performs a function similar to that of SV2 that mitigates the phenotype of SV2 knockout mice. To test this, we generated SVOP knockout mice and SVOP/SV2A/SV2B triple knockout mice. Mice lacking SVOP are viable, fertile and phenotypically normal. Measures of neurotransmission and behaviors dependent on the cerebellum and pineal gland revealed no measurable phenotype. SVOP/SV2A/SV2B triple knockout mice did not display a phenotype more severe than mice harboring the SV2A/SV2B gene deletions. These findings support the interpretation that SVOP performs a unique, though subtle, function that is not necessary for survival under normal conditions. |
