Côté Jocelyn, Richard Stéphane
Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital and Department of Oncology, McGill University, Montréal, Québec H3T 1E2, Canada.
J Biol Chem. 2005 Aug 5;280(31):28476-83. doi: 10.1074/jbc.M414328200. Epub 2005 Jun 6.
The Tudor domain is an approximately 60-amino acid structure motif in search of a function. Herein we show that the Tudor domains of the spinal muscular atrophy gene product SMN, the splicing factor 30 kDa (SPF30), and the Tudor domain-containing 3 (TDRD3) proteins interacted with arginine-glycine-rich motifs in a methylarginine-dependent manner. The Tudor domains also associated with methylarginine-containing cellular proteins, providing evidence that methylated arginines represent physiological ligands for this protein module. In addition, we report that spliceosomal small nuclear ribonucleoprotein particles core Sm proteins accumulated in the cytoplasm when arginine methylation was inhibited with adenosine dialdehyde or in the presence of an excessive amount of unmethylated arginine-glycine-rich peptides. These data provide in vivo evidence in support of a role for arginine methylation in the proper assembly and localization of spliceosomal Sm proteins.
Tudor结构域是一种寻找功能的约60个氨基酸的结构基序。在此我们表明,脊髓性肌萎缩症基因产物SMN、剪接因子30 kDa(SPF30)和含Tudor结构域3(TDRD3)蛋白的Tudor结构域以甲基精氨酸依赖性方式与富含精氨酸-甘氨酸的基序相互作用。Tudor结构域还与含甲基精氨酸的细胞蛋白相关联,这表明甲基化精氨酸是该蛋白模块的生理配体。此外,我们报告,当用腺苷二醛抑制精氨酸甲基化或在存在过量未甲基化的富含精氨酸-甘氨酸的肽时,剪接体小核核糖核蛋白颗粒核心Sm蛋白在细胞质中积累。这些数据提供了体内证据,支持精氨酸甲基化在剪接体Sm蛋白的正确组装和定位中的作用。