Epigenetic programming via histone methylation at WRKY53 controls leaf senescence in Arabidopsis thaliana
Epigenetic programming via histone methylation at WRKY53 controls leaf senescence in Arabidopsis thaliana
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DOI：
10.1111/j.0960-7412.2009.03782.x
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发表时间：
2009-04-01
期刊：
影响因子：
7.2
通讯作者：
Humbeck, Klaus
中科院分区：
文献类型：
--
作者：
Ay, Nicole;Irmler, Kristina;Humbeck, Klaus
叶片衰老是叶片发育的最后一步，涉及基因表达的广泛重编程。在这里，我们表明，这些过程包括离散变化的表观遗传索引，以及全球改变染色质组织。在叶片衰老过程中，间期核显示出染色中心异染色质的解凝聚，并且H3K4me2、H3K4me3以及H3K27me2和H3K27me3组蛋白修饰标记的核分布的变化分别指示活性和非活性染色质。在叶片衰老的关键调节子WRKY53上研究了基因座特异性表观遗传索引。在衰老过程中，当基因座被激活时，H3K4me2和H3K4me3在5'端和编码区显著增加。在过表达SUVH2组蛋白甲基转移酶的植物中观察到这些过程的损害，这导致异位异染色质化。在这些植物中，WRKY53和衰老相关基因SIRK、SAG101、ANAC083、SAG12和SAG24的转录起始被抑制，导致叶片衰老延迟。在SUVH 2过表达植物中，在WRKY53的5 '端区域检测到显著水平的H3K27me2和H3K27me3，导致其转录抑制。此外，SUVH 2过表达抑制衰老相关的染色质组织的整体变化。我们的数据表明，复杂的表观遗传过程控制衰老特异性基因表达模式。
Leaf senescence, the final step of leaf development, involves extensive reprogramming of gene expression. Here, we show that these processes include discrete changes of epigenetic indexing, as well as global alterations in chromatin organization. During leaf senescence, the interphase nuclei show a decondensation of chromocenter heterochromatin, and changes in the nuclear distribution of the H3K4me2, H3K4me3, and the H3K27me2 and H3K27me3 histone modification marks that index active and inactive chromatin, respectively. Locus-specific epigenetic indexing was studied at the WRKY53 key regulator of leaf senescence. During senescence, when the locus becomes activated, H3K4me2 and H3K4me3 are significantly increased at the 5' end and at coding regions. Impairment of these processes is observed in plants overexpressing the SUVH2 histone methyltransferase, which causes ectopic heterochromatization. In these plants the transcriptional initiation of WRKY53 and of the senescence-associated genes SIRK, SAG101, ANAC083, SAG12 and SAG24 is inhibited, resulting in a delay of leaf senescence. In SUVH2 overexpression plants, significant levels of H3K27me2 and H3K27me3 are detected at the 5'-end region of WRKY53, resulting in its transcriptional repression. Furthermore, SUVH2 overexpression inhibits senescence-associated global changes in chromatin organization. Our data suggest that complex epigenetic processes control the senescence-specific gene expression pattern.