Appleman Leonard J, Chernova Irina, Li Lequn, Boussiotis Vassiliki A
Department of Medical Oncology, Dana-Farber Cancer Institute, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Cell Cycle. 2006 Sep;5(18):2123-9. doi: 10.4161/cc.5.18.3139. Epub 2006 Sep 15.
Activation through TCR/CD3-plus-CD28 induces primary T lymphocytes to enter S phase. Downregulation of cyclin-dependent kinase inhibitor p27(kip1) is critical in this process and is mediated by ubiquitin-targeted degradation of p27(kip1). Ubiquitination of p27(kip1) is performed by the SCF(skp2) ubiquitin ligase comprised of the core components Roc1, Cul1 and Skp1 and the substrate recognition components Skp2 and Cks1. Here we show that in primary human T lymphocytes, the SCF(skp2) core components Roc1, Cul1 and Skp1 are constitutively expressed, and their levels remain unchanged upon TCR/CD3-plus-CD28 costimulation. In contrast, the substrate recognition components Skp2 and Cks1 are almost undetectable in resting T cells and are transcriptionally induced upon costimulation. We determined that the SKP2 promoter lies directly upstream of the translational start site and contains binding sites for SP1, Elk-1 and E2F transcription factors. Mutagenesis of SP1 and Elk-1 sites abrogated TCR/CD3-plus-CD28-mediated SKP2 promoter-driven reporter activity, whereas mutagenesis of an E2F site enhanced reporter activity, suggesting that SKP2 promoter may act as a node of integration for mitogenic and anti-mitogenic signals. Thus, in primary T lymphocytes CD28 costimulation can directly regulate cell cycle progression by inducing transcription of the substrate recognition components of SCF(skp2) ubiquitin ligase that targets p27(kip1) for degradation.
通过TCR/CD3加CD28激活可诱导原代T淋巴细胞进入S期。细胞周期蛋白依赖性激酶抑制剂p27(kip1)的下调在此过程中至关重要,并且由p27(kip1)的泛素靶向降解介导。p27(kip1)的泛素化由SCF(skp2)泛素连接酶执行,该连接酶由核心成分Roc1、Cul1和Skp1以及底物识别成分Skp2和Cks1组成。在这里,我们表明,在原代人T淋巴细胞中,SCF(skp2)核心成分Roc1、Cul1和Skp1组成性表达,并且它们的水平在TCR/CD3加CD28共刺激后保持不变。相反,底物识别成分Skp2和Cks1在静息T细胞中几乎检测不到,并且在共刺激后被转录诱导。我们确定SKP2启动子直接位于翻译起始位点的上游,并且包含SP1、Elk-1和E2F转录因子的结合位点。SP1和Elk-1位点的诱变消除了TCR/CD3加CD28介导的SKP2启动子驱动的报告基因活性,而E2F位点的诱变增强了报告基因活性,这表明SKP2启动子可能作为有丝分裂和抗有丝分裂信号整合的节点。因此,在原代T淋巴细胞中,CD28共刺激可通过诱导靶向p27(kip1)进行降解的SCF(skp2)泛素连接酶的底物识别成分的转录来直接调节细胞周期进程。