| First Author | Raman AV | Year | 2012 |
| Journal | Genes Brain Behav | Volume | 11 |
| Issue | 5 | Pages | 601-13 |
| PubMed ID | 22487427 | Mgi Jnum | J:191114 |
| Mgi Id | MGI:5460964 | Doi | 10.1111/j.1601-183X.2012.00794.x |
| Citation | Raman AV, et al. (2012) Absence of selenoprotein P but not selenocysteine lyase results in severe neurological dysfunction. Genes Brain Behav 11(5):601-13 |
| abstractText | Dietary selenium restriction in mammals causes bodily selenium to be preferentially retained in the brain relative to other organs. Almost all the known selenoproteins are found in brain, where expression is facilitated by selenocysteine (Sec)-laden selenoprotein P. The brain also expresses selenocysteine lyase (Scly), an enzyme that putatively salvages Sec and recycles the selenium for selenoprotein translation. We compared mice with a genetic deletion of Scly to selenoprotein P (Sepp1) knockout mice for similarity of neurological impairments and whether dietary selenium modulates these parameters. We report that Scly knockout mice do not display neurological dysfunction comparable to Sepp1 knockout mice. Feeding a low-selenium diet to Scly knockout mice revealed a mild spatial learning deficit without disrupting motor coordination. Additionally, we report that the neurological phenotype caused by the absence of Sepp1 is exacerbated in male vs. female mice. These findings indicate that Sec recycling via Scly becomes limiting under selenium deficiency and suggest the presence of a complementary mechanism for processing Sec. Our studies illuminate the interaction between Sepp1 and Scly in the distribution and turnover of body and brain selenium and emphasize the consideration of sex differences when studying selenium and selenoproteins in vertebrate biology. |
