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多唾液酸转移酶与神经细胞黏附分子的两个结构域中的序列相互作用,从而允许其进行多唾液酸化。

The polysialyltransferases interact with sequences in two domains of the neural cell adhesion molecule to allow its polysialylation.

机构信息

Department of Biochemistry and Molecular Genetics, University of Illinois, College of Medicine, Chicago, Illinois 60607, USA.

出版信息

J Biol Chem. 2013 Mar 8;288(10):7282-93. doi: 10.1074/jbc.M112.438374. Epub 2013 Jan 22.

Abstract

The neural cell adhesion molecule (NCAM) is the major substrate for the polysialyltransferases (polySTs), ST8SiaII/STX and ST8SiaIV/PST. The polysialylation of NCAM N-glycans decreases cell adhesion and alters signaling. Previous work demonstrated that the first fibronectin type III repeat (FN1) of NCAM is required for polyST recognition and the polysialylation of the N-glycans on the adjacent Ig5 domain. In this work, we highlight the importance of an FN1 acidic patch in polyST recognition and also reveal that the polySTs are required to interact with sequences in the Ig5 domain for polysialylation to occur. We find that features of the Ig5 domain of the olfactory cell adhesion molecule (OCAM) are responsible for its lack of polysialylation. Specifically, two basic OCAM Ig5 residues (Lys and Arg) found near asparagines equivalent to those carrying the polysialylated N-glycans in NCAM substantially decrease or eliminate polysialylation when used to replace the smaller and more neutral residues (Ser and Asn) in analogous positions in NCAM Ig5. This decrease in polysialylation does not reflect altered glycosylation but instead is correlated with a decrease in polyST-NCAM binding. In addition, inserting non-conserved OCAM sequences into NCAM Ig5, including an "extra" N-glycosylation site, decreases or completely blocks NCAM polysialylation. Taken together, these results indicate that the polySTs not only recognize an acidic patch in the FN1 domain of NCAM but also must contact sequences in the Ig5 domain for polysialylation of Ig5 N-glycans to occur.

摘要

神经细胞黏附分子 (NCAM) 是多唾液酸转移酶 (polyST)、ST8SiaII/STX 和 ST8SiaIV/PST 的主要底物。NCAM N-糖链的多唾液酸化会降低细胞黏附性并改变信号转导。先前的工作表明,NCAM 的第一个纤维连接蛋白 III 型重复 (FN1) 是多 ST 识别和相邻 Ig5 结构域上 N-糖链多唾液酸化所必需的。在这项工作中,我们强调了 FN1 酸性斑在多 ST 识别中的重要性,还揭示了多 ST 与 Ig5 结构域中的序列相互作用对于多唾液酸化的发生是必需的。我们发现嗅球细胞黏附分子 (OCAM) 的 Ig5 结构域的特征决定了其缺乏多唾液酸化。具体来说,在 NCAM Ig5 中与多唾液酸化 N-糖链等效的位置附近存在两个碱性 OCAM Ig5 残基(赖氨酸和精氨酸),当它们取代 NCAM Ig5 中类似位置的较小且更中性的残基(丝氨酸和天冬酰胺)时,会大大减少或消除多唾液酸化。这种多唾液酸化的减少不是由于糖基化改变,而是与多 ST-NCAM 结合减少相关。此外,将非保守的 OCAM 序列插入 NCAM Ig5 中,包括一个“额外”的 N-糖基化位点,会减少或完全阻止 NCAM 多唾液酸化。综上所述,这些结果表明,多 ST 不仅识别 NCAM FN1 结构域中的酸性斑,而且还必须与 Ig5 结构域中的序列相互作用才能使 Ig5 N-糖链发生多唾液酸化。

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