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组蛋白 H3K4 去甲基化酶 JMJ16 抑制拟南芥叶片衰老。

The Histone H3K4 Demethylase JMJ16 Represses Leaf Senescence in Arabidopsis.

机构信息

Key Laboratory of Plant Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China.

State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.

出版信息

Plant Cell. 2019 Feb;31(2):430-443. doi: 10.1105/tpc.18.00693. Epub 2019 Feb 1.

DOI:10.1105/tpc.18.00693
PMID:30712008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6447021/
Abstract

Leaf senescence is governed by a complex regulatory network involving the dynamic reprogramming of gene expression. Age-dependent induction of senescence-associated genes (SAGs) is associated with increased levels of trimethylation of histone H3 at Lys4 (H3K4me3), but the regulatory mechanism remains elusive. Here, we found that JMJ16, an Arabidopsis () JmjC-domain containing protein, is a specific H3K4 demethylase that negatively regulates leaf senescence through its enzymatic activity. Genome-wide analysis revealed a widespread coordinated upregulation of gene expression and hypermethylation of H3K4me3 at JMJ16 binding genes associated with leaf senescence in the loss-of-function mutant as compared with the wild type. Genetic analysis indicated that JMJ16 negatively regulates leaf senescence, at least partly through repressing the expression of positive regulators of leaf senescence, and JMJ16 associates with and and represses their precocious expression in mature leaves by reducing H3K4me3 levels at these loci. The protein abundance of JMJ16 gradually decreases during aging, which is correlated with increased H3K4me3 levels at and , suggesting that the age-dependent downregulation of JMJ16 is required for the precise transcriptional activation of SAGs during leaf senescence. Thus, JMJ16 is an important regulator of leaf senescence that demethylates H3K4 at SAGs in an age-dependent manner.

摘要

叶片衰老受一个复杂的调控网络控制,该网络涉及基因表达的动态重编程。与衰老相关基因(SAGs)的年龄依赖性诱导与组蛋白 H3 在赖氨酸 4 位的三甲基化(H3K4me3)水平升高有关,但调控机制仍不清楚。在这里,我们发现拟南芥(Arabidopsis)中的 JMJ16 是一种含有 JmjC 结构域的蛋白,是一种特异性的 H3K4 去甲基化酶,通过其酶活性负调控叶片衰老。全基因组分析显示,与野生型相比,功能丧失突变体中与叶片衰老相关的 JMJ16 结合基因的表达广泛上调,并伴随着 H3K4me3 的超甲基化。遗传分析表明,JMJ16 负调控叶片衰老,至少部分是通过抑制叶片衰老的正调控因子的表达来实现的,JMJ16 与和 JMJ16 结合,并通过降低这些基因座上的 H3K4me3 水平来抑制它们在成熟叶片中的过早表达。JMJ16 的蛋白丰度在衰老过程中逐渐降低,与和 上 H3K4me3 水平的升高相关,这表明 JMJ16 的年龄依赖性下调是 SAGs 在叶片衰老过程中精确转录激活所必需的。因此,JMJ16 是叶片衰老的一个重要调控因子,它以年龄依赖的方式使 SAGs 上的 H3K4 去甲基化。

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