Glycobiology Advance Access originally published online on April 22, 2009
Glycobiology 2009 19(8):879-889; doi:10.1093/glycob/cwp062
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Glycosylation-related gene expression profiling in the brain and spleen of scrapie-affected mouse
2 INRA, UMR1061 Génétique Moléculaire Animale – Université de Limoges, F-87060 Limoges, France
3 CNRS, UMR 6101 Physiologie Moléculaire de la Réponse Immune et des Lymphoproliférations – Université de Limoges, F-87025 Limoges, France
4 INRA, UR1313 Génétique Animale et Biologie Intégrative, F-78350 Jouy-en-Josas, France
5 EA 4169 Université Lyon-1, Hopital Edouard Herriot, F-69000 Lyon, France
6 Institute of Macromolecular Chemistry, Iasi, Romania
7 INRA, UR892 Virologie Immunologie Moléculaires, F-78350 Jouy-en-Josas, France
1 To whom correspondence should be addressed: Tel: 335-5545-7654; Fax: 335-5545-7653; e-mail: francois.gallet{at}unilim.fr
Received on December 18, 2008; revised on April 17, 2009; accepted on April 18, 2009
A central event in the formation of infectious prions is the conformational change of a host-encoded glycoprotein, PrPC, into a pathogenic isoform, PrPSc. The molecular requirements for efficient PrP conversion remain unknown. Altered glycosylation has been linked to various pathologies and the N-glycans harbored by two prion protein isoforms are different. In order to search for glycosylation-related genes that could mark prion infection, we used a glycosylation-dedicated microarray that allowed the simultaneous analysis of the expression of 165 glycosylation-related genes encoding proteins of the glycosyltransferase, glycosidase, lectin, and sulfotransferase families to compare the gene expression profiles of normal and scrapie-infected mouse brain and spleen. Eight genes were found upregulated in "scrapie brain" at the final state of the disease. In the spleen, five genes presented a modified expression. Three genes were also upregulated in the spleen of infected mice, and two (Pigq and St3gal5) downregulated. All changes were confirmed by qPCR and biochemical analyses applied to Pigq and St3gal5 proteins.
Key words: brain / gene expression / microarray / prion disease / spleen