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拟南芥染色质重塑因子 PICKLE 与转录因子 HY5 相互作用,调节下胚轴细胞伸长。

Arabidopsis chromatin remodeling factor PICKLE interacts with transcription factor HY5 to regulate hypocotyl cell elongation.

机构信息

Key Laboratory of Photobiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.

出版信息

Plant Cell. 2013 Jan;25(1):242-56. doi: 10.1105/tpc.112.105742. Epub 2013 Jan 11.

Abstract

Photomorphogenesis is a critical plant developmental process that involves light-mediated transcriptome changes, histone modifications, and inhibition of hypocotyl growth. However, the chromatin-based regulatory mechanism underlying this process remains largely unknown. Here, we identify ENHANCED PHOTOMORPHOGENIC1 (EPP1), previously known as PICKLE (PKL), an ATP-dependent chromatin remodeling factor of the chromodomain/helicase/DNA binding family, as a repressor of photomorphogenesis in Arabidopsis thaliana. We show that PKL/EPP1 expression is repressed by light in the hypocotyls in a photoreceptor-dependent manner. Furthermore, we reveal that the transcription factor ELONGATED HYPOCOTYL5 (HY5) binds to the promoters of cell elongation-related genes and recruits PKL/EPP1 through their physical interaction. PKL/EPP1 in turn negatively regulates HY5 by repressing trimethylation of histone H3 Lys 27 at the target loci, thereby regulating the expression of these genes and, thus, hypocotyl elongation. We also show that HY5 possesses transcriptional repression activity. Our study reveals a crucial role for a chromatin remodeling factor in repressing photomorphogenesis and demonstrates that transcription factor-mediated recruitment of chromatin-remodeling machinery is important for plant development in response to changing light environments.

摘要

光形态建成是一个关键的植物发育过程,涉及光介导的转录组变化、组蛋白修饰和抑制下胚轴生长。然而,这一过程背后的基于染色质的调控机制在很大程度上仍然未知。在这里,我们鉴定出先前被称为 PICKLE (PKL) 的增强光形态建成 1 (EPP1),作为拟南芥光形态建成的抑制因子,它是一个依赖于 ATP 的染色质重塑因子,属于 chromodomain/helicase/DNA 结合家族。我们表明,PKL/EPP1 的表达在光下被下胚轴中的光受体以依赖于光受体的方式抑制。此外,我们揭示了转录因子伸长下胚轴 5 (HY5) 结合到与细胞伸长相关基因的启动子上,并通过它们的物理相互作用招募 PKL/EPP1。PKL/EPP1 反过来通过抑制靶位上组蛋白 H3 赖氨酸 27 的三甲基化来负调控 HY5,从而调节这些基因的表达,进而调节下胚轴的伸长。我们还表明,HY5 具有转录抑制活性。我们的研究揭示了染色质重塑因子在抑制光形态建成中的关键作用,并表明转录因子介导的染色质重塑机制的募集对于植物在应对不断变化的光照环境时的发育是很重要的。

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