Ito Jun, Fukaki Hidehiro, Onoda Makoto, Li Lin, Li Chuanyou, Tasaka Masao, Furutani Masahiko
Graduate School of Biological Sciences, Nara Institute of Science and Technology, Nara 630-0192, Japan;
Department of Biology, Graduate School of Science, Kobe University, Kobe 657-8501, Japan;
Proc Natl Acad Sci U S A. 2016 Jun 7;113(23):6562-7. doi: 10.1073/pnas.1600739113. Epub 2016 May 23.
Mediator is a multiprotein complex that integrates the signals from transcription factors binding to the promoter and transmits them to achieve gene transcription. The subunits of Mediator complex reside in four modules: the head, middle, tail, and dissociable CDK8 kinase module (CKM). The head, middle, and tail modules form the core Mediator complex, and the association of CKM can modify the function of Mediator in transcription. Here, we show genetic and biochemical evidence that CKM-associated Mediator transmits auxin-dependent transcriptional repression in lateral root (LR) formation. The AUXIN/INDOLE 3-ACETIC ACID 14 (Aux/IAA14) transcriptional repressor inhibits the transcriptional activity of its binding partners AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19 by making a complex with the CKM-associated Mediator. In addition, TOPLESS (TPL), a transcriptional corepressor, forms a bridge between IAA14 and the CKM component MED13 through the physical interaction. ChIP assays show that auxin induces the dissociation of MED13 but not the tail module component MED25 from the ARF7 binding region upstream of its target gene. These findings indicate that auxin-induced degradation of IAA14 changes the module composition of Mediator interacting with ARF7 and ARF19 in the upstream region of their target genes involved in LR formation. We suggest that this regulation leads to a quick switch of signal transmission from ARFs to target gene expression in response to auxin.
中介体是一种多蛋白复合物，它整合来自与启动子结合的转录因子的信号并将其传递以实现基因转录。中介体复合物的亚基存在于四个模块中：头部、中部、尾部和可解离的细胞周期蛋白依赖性激酶8激酶模块（CKM）。头部、中部和尾部模块形成核心中介体复合物，CKM的结合可以改变中介体在转录中的功能。在这里，我们展示了遗传和生化证据，表明与CKM相关的中介体在侧根形成中传递生长素依赖性转录抑制。生长素/吲哚-3-乙酸14（Aux/IAA14）转录抑制因子通过与与CKM相关的中介体形成复合物来抑制其结合伙伴生长素响应因子7（ARF7）和ARF19的转录活性。此外，转录共抑制因子TOPLESS（TPL）通过物理相互作用在IAA14和CKM组分MED13之间形成桥梁。染色质免疫沉淀分析表明，生长素诱导MED13从其靶基因上游的ARF7结合区域解离，但不诱导尾部模块组分MED25解离。这些发现表明，生长素诱导的IAA14降解改变了在侧根形成相关靶基因上游区域与ARF7和ARF19相互作用的中介体的模块组成。我们认为这种调节导致了响应生长素时信号从ARF传递到靶基因表达的快速转换。
