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HNK‐1 sulfotransferase null mice express glucuronyl glycoconjugates and show normal cerebellar granule neuron migration in vivo and in vitro
Author(s) -
Chou Denise K. H.,
Schachner Melitta,
Jungalwala Firoze B.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.01066.x
Subject(s) - glycolipid , neurite , microbiology and biotechnology , glycoconjugate , mutant , biology , glycoprotein , in vivo , biochemistry , in vitro , central nervous system , chemistry , neuroscience , gene , genetics
Sulfoglucuronyl carbohydrate (SGC), reactive with antibody against human natural killer cell antigen, is expressed in several glycolipids, glycoproteins and proteoglycans of the nervous system and has been implicated in cell–cell recognition, neurite outgrowth and neuronal migration during development, through its interaction with SGC‐binding protein (SBP) 1. However, sulfotransferase (ST) null mutant mice, which lack SGC, were shown to have normal development with usual gross anatomy of the nervous system and other organs. Failure to observe a severe phenotype in the ST null mice prompted us to determine the compensatory molecular replacement of SGC by analyzing the carbohydrate of glycolipids and glycoproteins of the ST mutant nervous system. In the ST null mice, SGC‐containing molecules were absent; instead the precursor glucuronyl carbohydrate (GC)‐containing molecules accumulated. Other relevant glycolipids and proteins were not affected. The GC molecules in the mutant were localized at the same anatomical sites in the nervous system as the SGC molecules in the wild type. In vitro binding studies showed that, similar to sulfoglucuronyl glycolipids, glucuronyl glycolipids interacted with SBP‐1, but with a lower binding capacity. In vitro studies with explant cultures of cerebellum indicated that neurite outgrowth and cell migration were not significantly affected in the mutant, possibly owing to interaction of SBP‐1 with GC molecules. The results suggested that in vivo SBP‐1–GC interaction was sufficient to allow normal neurite outgrowth and cell migration in the mutant, giving rise to a wild‐type phenotype. However, the role of other compensatory molecules involved in these processes cannot be completely ruled out.