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Published June 15, 2009 | Supplemental Material + Published
Journal Article Open

Identification of the Plasticity-Relevant Fucose-α(1−2)-Galactose Proteome from the Mouse Olfactory Bulb

Abstract

Fucose-α(1−2)-galactose [Fucα(1−2)Gal] sugars have been implicated in the molecular mechanisms that underlie neuronal development, learning, and memory. However, an understanding of their precise roles has been hampered by a lack of information regarding Fucα(1−2)Gal glycoproteins. Here, we report the first proteomic studies of this plasticity-relevant epitope. We identify five classes of putative Fucα(1−2)Gal glycoproteins: cell adhesion molecules, ion channels and solute carriers/transporters, ATP-binding proteins, synaptic vesicle-associated proteins, and mitochondrial proteins. In addition, we show that Fucα(1−2)Gal glycoproteins are enriched in the developing mouse olfactory bulb (OB) and exhibit a distinct spatiotemporal expression that is consistent with the presence of a "glycocode" to help direct olfactory sensory neuron (OSN) axonal pathfinding. We find that expression of Fucα(1−2)Gal sugars in the OB is regulated by the α(1−2)fucosyltransferase FUT1. FUT1-deficient mice exhibit developmental defects, including fewer and smaller glomeruli and a thinner olfactory nerve layer, suggesting that fucosylation contributes to OB development. Our findings significantly expand the number of Fucα(1−2)Gal glycoproteins and provide new insights into the molecular mechanisms by which fucosyl sugars contribute to neuronal processes.

Additional Information

© 2009 American Chemical Society. ACS AuthorChoice. Received April 15, 2009; Revised Manuscript Received June 15, 2009. The ASCS4 hybridoma developed by P. H. Patterson, the 5e hybridoma developed by U. Rutishauser, and the α5 hybridoma developed by P. M. Fambrough were obtained from the Developmental Studies Hybridoma Bank under the auspices of the National Institute of Child and Human Development and maintained by the Department of Biology, The University of Iowa, Iowa City, IA 52242. We thank John Lowe for contributing the FUT1- and FUT2-deficient mice used in this study. This research was supported by National Institutes of Health Grants RO1 GM084724-05 (L.C.H.-W.), T32 GM08501 (H.E.M.), and 5T32 GM07616-30S1 (C.K.).

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