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A more recent version of this article appeared on December 30, 2005
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M511097200v1
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Papers In Press, published online ahead of print November 2, 2005
J. Biol. Chem, 10.1074/jbc.M511097200
Submitted on October 12, 2005
Accepted on November 2, 2005

Genetic ablation of polysialic acid causes severe neurodevelopmental defects rescued by ncam deletion

Birgit Weinhold, Ralph Seidenfaden, Iris Röckle, Martina Mühlenhoff, Frank Schertzinger, Sidonie Conzelmann, Jamey D. Marth, Rita Gerardy-Schahn, and Herbert Hildebrandt

Abteilung Zelluläre Chemie, Medizinische Hochschule Hannover, Hannover 30625

Corresponding Author: gerardy-schahn.rita{at}mh-hannover.de

Poly-alpha-2,8-sialic acid (polySia ) is a unique modification of the neural cell adhesion molecule NCAM tightly associated with neural development and plasticity. However, the vital role attributed to this carbohydrate polymer has been challenged by the mild phenotype of mice lacking polySia due to NCAM-deficiency. To dissect polySia and NCAM functions, we generated polySia-negative but NCAM-positive mice by simultaneous deletion of the two polysialyltransferase genes St8sia-II and St8sia-IV. Beyond features shared with NCAM-null animals, a severe phenotype with specific brain wiring defects, progressive hydrocephalus, postnatal growth retardation, and precocious death was observed. These drastic defects were selectively rescued by additional deletion of NCAM, demonstrating that they originate from a gain of NCAM functions due to polySia-deficiency. The data presented in this study reveal that the essential role of polySia resides in the control and coordination of NCAM interactions during mouse brain development. Moreover, this first demonstration in vivo that a highly specific glycan structure is more important than the glycoconjugate as a whole provides a novel view on the relevance of protein glycosylation for the complex process of building the vertebrate brain.


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