Department of Pharmacology, University of California-San Diego , La Jolla, California 92093-0636, United States.
Biochemistry. 2013 Oct 29;52(43):7595-605. doi: 10.1021/bi4010864. Epub 2013 Oct 15.
The splicing function of SR proteins is regulated by multisite phosphorylation of their C-terminal RS (arginine-serine rich) domains. SRPK1 has been shown to phosphorylate the prototype SR protein SRSF1 using a directional mechanism in which 11 serines flanked by arginines are sequentially fed from a docking groove in the large lobe of the kinase domain to the active site. Although this process is expected to operate on lengthy arginine-serine repeats (≥8), many SR proteins contain smaller repeats of only 1-4 dipeptides, raising the question of how alternate RS domain configurations are phosphorylated. To address this, we studied a splice variant of Tra2β that contains a C-terminal RS domain with short arginine-serine repeats [Tra2β(ΔN)]. We showed that SRPK1 selectively phosphorylates several serines near the C-terminus of the RS domain. SRPK1 uses a distributive mechanism for Tra2β(ΔN) where the rate-limiting step is the dissociation of the protein substrate rather than nucleotide exchange as in the case of SRSF1. Although a functioning docking groove is required for efficient SRSF1 phosphorylation, this conserved structural element is dispensable for Tra2β(ΔN) phosphorylation. These large shifts in mechanism are likely to account for the slower net turnover rate of Tra2β(ΔN) compared to SRSF1 and may signal fundamental differences in phosphorylation among SR proteins with distinctive arginine-serine profiles. Overall, these data indicate that SRPK1 conforms to changes in RS domain architecture using a flexible kinetic mechanism and selective usage of a conserved docking groove.
SR 蛋白的剪接功能受其 C 端 RS(精氨酸-丝氨酸富含)结构域多位点磷酸化的调节。已经表明,SRPK1 通过定向机制磷酸化原型 SR 蛋白 SRSF1,其中 11 个被精氨酸包围的丝氨酸通过激酶结构域大亚基中的对接槽从一个停靠点顺序输送到活性位点。尽管这个过程预计会在长的精氨酸-丝氨酸重复序列(≥8)上起作用,但许多 SR 蛋白只含有 1-4 个二肽的较短重复序列,这就提出了如何磷酸化替代 RS 结构域构型的问题。为了解决这个问题,我们研究了一种含有短精氨酸-丝氨酸重复序列的 Tra2β 剪接变体[Tra2β(ΔN)]。我们表明,SRPK1 选择性地磷酸化 RS 结构域 C 端附近的几个丝氨酸。SRPK1 对 Tra2β(ΔN) 使用分布机制,其限速步骤是蛋白质底物的解离,而不是如 SRSF1 情况下的核苷酸交换。虽然有效的对接槽是 SRSF1 磷酸化所必需的,但这个保守的结构元件对于 Tra2β(ΔN)的磷酸化是可有可无的。这些机制的巨大转变可能解释了 Tra2β(ΔN)与 SRSF1 相比较慢的净周转率,并可能表明具有不同精氨酸-丝氨酸谱的 SR 蛋白在磷酸化方面存在根本差异。总的来说,这些数据表明,SRPK1 通过使用灵活的动力学机制和选择性使用保守的对接槽来适应 RS 结构域架构的变化。