Binda O, Nassif C, Branton P E
Department of Biochemistry, McGill University, Montréal, Québec, Canada.
Oncogene. 2008 May 29;27(24):3384-92. doi: 10.1038/sj.onc.1211014. Epub 2008 Jan 14.
Both RBP1 and the highly related protein BCAA play a role in the induction of growth arrest and cellular senescence via mechanisms involving transcriptional repression. While investigating the transcriptional repression activities of RBP1, we observed a genetic link between RBP1 and SIR2. Further work uncovered an interaction between RBP1 family proteins and the mammalian homologue of SIR2, SIRT1. Interestingly, the HDAC-dependent transcriptional repression domain of RBP1 proteins, termed R2, is necessary and sufficient for the interaction with SIRT1. In vitro and in vivo binding studies indicated that the p33(ING1b) and p33(ING2) subunits of the mSIN3A/HDAC1 complex are responsible for the recruitment of SIRT1 to the R2 domain. To investigate the biological relevance of this interaction, we used the sirtuin activator resveratrol and the sirtuin inhibitor sirtinol in transcriptional repression assays and demonstrated that SIRT1 activity negatively regulates R2-mediated transcriptional repression activity. We therefore propose a novel mechanism of class I HDAC regulation by a class III HDAC. Explicitly, SIRT1 is recruited by ING proteins and inhibits R2-associated mSIN3A/HDAC1 transcriptional repression activity.
RBP1和高度相关的蛋白质BCAA均通过涉及转录抑制的机制在诱导生长停滞和细胞衰老中发挥作用。在研究RBP1的转录抑制活性时,我们观察到RBP1与SIR2之间存在遗传联系。进一步的研究发现了RBP1家族蛋白与SIR2的哺乳动物同源物SIRT1之间的相互作用。有趣的是,RBP1蛋白的依赖HDAC的转录抑制结构域(称为R2)对于与SIRT1的相互作用是必要且充分的。体外和体内结合研究表明,mSIN3A/HDAC1复合物的p33(ING1b)和p33(ING2)亚基负责将SIRT1募集到R2结构域。为了研究这种相互作用的生物学意义,我们在转录抑制试验中使用了sirtuin激活剂白藜芦醇和sirtuin抑制剂sirtinol,并证明SIRT1活性负向调节R2介导的转录抑制活性。因此,我们提出了一种由III类HDAC调节I类HDAC的新机制。具体而言,SIRT1被ING蛋白募集并抑制与R2相关的mSIN3A/HDAC1转录抑制活性。