Carey D J, Bendt K M, Stahl R C
Sigfried and Janet Weis Center for Research, Geisinger Clinic, Danville, Pennsylvania 17822, USA.
J Biol Chem. 1996 Jun 21;271(25):15253-60. doi: 10.1074/jbc.271.25.15253.
Syndecan-1 is a member of a gene family of multifunctional transmembrane heparan sulfate proteoglycans that bind a variety of extracellular ligands and possess highly conserved non-catalytic cytoplasmic domains. It has been shown that antibody-mediated clustering of syndecan-1 causes the proteoglycan to become associated with microfilaments and insoluble in non-ionic detergent. A series of truncation and point mutations of the syndecan-1 core protein was constructed to identify specific structural features that were required for these characteristics. The transmembrane domain but not the cytoplasmic domain was required for cell surface expression of syndecan-1. Deletion of the COOH-terminal 11 amino acids of the cytoplasmic domain had no effect, while deletion of an additional 12 amino acids abolished microfilament association. Mutation of a conserved tyrosine residue within the latter region also abolished microfilament association. In contrast, mutation of 2 tyrosine residues outside this region had no effect. Deletion of the entire cytoplasmic domain (except for a short stop-transfer sequence) did not affect insolubility of the proteoglycan in detergent. Analysis of a form of syndecan-1 that lacked glycosaminoglycan acceptor sites revealed that covalently attached glycosaminoglycans were not required for cell surface expression, microfilament association, or detergent insolubility. These results demonstrate that microfilament association is a function of a subregion within the cytoplasmic domain and suggest that insolubility in detergent is a function of the transmembrane domain.
Syndecan-1是多功能跨膜硫酸乙酰肝素蛋白聚糖基因家族的成员,该家族可结合多种细胞外配体,并拥有高度保守的非催化性胞质结构域。研究表明,抗体介导的Syndecan-1聚集会使蛋白聚糖与微丝结合,并使其不溶于非离子去污剂。构建了一系列Syndecan-1核心蛋白的截短突变体和点突变体,以确定这些特性所需的特定结构特征。Syndecan-1的细胞表面表达需要跨膜结构域而非胞质结构域。胞质结构域COOH末端11个氨基酸的缺失没有影响,而额外12个氨基酸的缺失则消除了与微丝的结合。该区域内一个保守酪氨酸残基的突变也消除了与微丝的结合。相比之下,该区域外2个酪氨酸残基的突变没有影响。整个胞质结构域(除了一个短的停止转移序列)的缺失并不影响蛋白聚糖在去污剂中的不溶性。对缺乏糖胺聚糖受体位点的Syndecan-1形式的分析表明,共价连接的糖胺聚糖对于细胞表面表达、微丝结合或去污剂不溶性不是必需的。这些结果表明,微丝结合是胞质结构域内一个亚区域的功能,并表明在去污剂中的不溶性是跨膜结构域的功能。