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转录共抑制因子LEUNIG与组蛋白去乙酰化酶HDA19以及中介体成分MED14(SWP)和CDK8(HEN3)相互作用以抑制转录。

The transcription corepressor LEUNIG interacts with the histone deacetylase HDA19 and mediator components MED14 (SWP) and CDK8 (HEN3) to repress transcription.

作者信息

Gonzalez Deyarina, Bowen Adam J, Carroll Thomas S, Conlan R Steven

机构信息

Institute of Life Science, School of Medicine, University of Wales Swansea, Singleton Park, Swansea SA2 8PP, United Kingdom.

出版信息

Mol Cell Biol. 2007 Aug;27(15):5306-15. doi: 10.1128/MCB.01912-06. Epub 2007 May 25.

Abstract

Transcription corepressors are general regulators controlling the expression of genes involved in multiple signaling pathways and developmental programs. Repression is mediated through mechanisms including the stabilization of a repressive chromatin structure over control regions and regulation of Mediator function inhibiting RNA polymerase II activity. Using whole-genome arrays we show that the Arabidopsis thaliana corepressor LEUNIG, a member of the GroTLE transcription corepressor family, regulates the expression of multiple targets in vivo. LEUNIG has a role in the regulation of genes involved in a number of different physiological processes including disease resistance, DNA damage response, and cell signaling. We demonstrate that repression of in vivo LEUNIG targets is achieved through histone deacetylase (HDAC)-dependent and -independent mechanisms. HDAC-dependent mechanisms involve direct interaction with HDA19, a class 1 HDAC, whereas an HDAC-independent repression activity involves interactions with the putative Arabidopsis Mediator components AtMED14/SWP and AtCDK8/HEN3. We suggest that changes in chromatin structure coupled with regulation of Mediator function are likely to be utilized by LEUNIG in the repression of gene transcription.

摘要

转录共抑制因子是控制参与多种信号通路和发育程序的基因表达的通用调节因子。抑制作用通过多种机制介导,包括在控制区域稳定抑制性染色质结构以及调节中介体功能以抑制RNA聚合酶II的活性。利用全基因组阵列,我们发现拟南芥共抑制因子LEUNIG(GroTLE转录共抑制因子家族的成员)在体内调节多个靶标的表达。LEUNIG在调控涉及多种不同生理过程的基因中发挥作用,这些生理过程包括抗病性、DNA损伤反应和细胞信号传导。我们证明,体内LEUNIG靶标的抑制是通过组蛋白脱乙酰酶(HDAC)依赖性和非依赖性机制实现的。HDAC依赖性机制涉及与1类HDAC HDA19的直接相互作用,而HDAC非依赖性抑制活性涉及与推定的拟南芥中介体组分AtMED14/SWP和AtCDK8/HEN3的相互作用。我们认为,LEUNIG可能利用染色质结构的变化以及中介体功能的调节来抑制基因转录。

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