Phosphatidylinositol 5-phosphate links dehydration stress to the activity of ARABIDOPSIS TRITHORAX-LIKE factor ATX1.
Phosphatidylinositol 5-phosphate links dehydration stress to the activity of ARABIDOPSIS TRITHORAX-LIKE factor ATX1.
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DOI：
10.1371/journal.pone.0013396
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发表时间：
2010-10-13
期刊：
影响因子：
3.7
通讯作者：
Avramova Z
中科院分区：
文献类型：
--
作者：
Ndamukong I;Jones DR;Lapko H;Divecha N;Avramova Z
基因表达的变化使生物体能够对环境压力做出反应。细胞脂质第二信使（例如磷酸肌醇 PtdIns5P）的水平会响应各种应激而发生变化，并且可以调节许多细胞内蛋白质的定位、构象和活性。植物三胸因子 (ATX1) 在基因编码序列处对组蛋白 H3 (H3K4me3) 的赖氨酸 4 残基进行三甲基化，这与基因转录呈正相关。微阵列分析已鉴定出拟南芥中受 ATX1 和外源添加 PtdIns5P 调节的靶基因 (WRKY70)。有趣的是，ATX1 含有 PtdIns5P 相互作用结构域（PHD 指），因此磷酸肌醇信号传导可能将环境压力与基因转录的变化联系起来。使用植物拟南芥作为模型系统，我们证明了 PtdIns5P 与染色质修饰剂 ATX1 响应脱水应激的活性之间的联系。我们首次表明，脱水会导致拟南芥细胞中 PtdIns5P 的增加。拟南芥肌管蛋白同源物 (AtMTM1) 能够产生 PtdIns5P，在这里，我们表明 AtMTM1 对于脱水时诱导 PtdIns5P 的增加至关重要。此外，我们证明 ATX1 依赖性基因 WRKY70 在脱水过程中下调，并且转录水平降低伴随着其核小体 H3K4me3 的急剧减少。我们以 WRKY70 核小体 K4 甲基化的变化为模型来研究脱水应激期间染色质上的 ATX1 活性。我们发现，在脱水应激期间，WRKY70 基因座上 ATX1 的物理存在减少，并且当 PtdIns5P 升高时，ATX1 因保留在细胞质中而导致 ATX1 耗尽。 ATX1 的 PHD 和催化活性 AtMTM1 是 ATX1 细胞质定位所必需的。该手稿的新颖之处在于发现了信号通路中染色质修饰活性（ATX1）和脂质（PtdIns5P）合成之间的机制联系，最终导致响应脱水应激而下调的 ATX1 依赖基因的表达改变。
Changes in gene expression enable organisms to respond to environmental stress. Levels of cellular lipid second messengers, such as the phosphoinositide PtdIns5P, change in response to a variety of stresses and can modulate the localization, conformation and activity of a number of intracellular proteins. The plant trithorax factor (ATX1) tri-methylates the lysine 4 residue of histone H3 (H3K4me3) at gene coding sequences, which positively correlates with gene transcription. Microarray analysis has identified a target gene (WRKY70) that is regulated by both ATX1 and by the exogenous addition of PtdIns5P in Arabidopsis. Interestingly, ATX1 contains a PtdIns5P interaction domain (PHD finger) and thus, phosphoinositide signaling, may link environmental stress to changes in gene transcription. Using the plant Arabidopsis as a model system, we demonstrate a link between PtdIns5P and the activity of the chromatin modifier ATX1 in response to dehydration stress. We show for the first time that dehydration leads to an increase in cellular PtdIns5P in Arabidopsis. The Arabidopsis homolog of myotubularin (AtMTM1) is capable of generating PtdIns5P and here, we show that AtMTM1 is essential for the induced increase in PtdIns5P upon dehydration. Furthermore, we demonstrate that the ATX1-dependent gene, WRKY70, is downregulated during dehydration and that lowered transcript levels are accompanied by a drastic reduction in H3K4me3 of its nucleosomes. We follow changes in WRKY70 nucleosomal K4 methylation as a model to study ATX1 activity at chromatin during dehydration stress. We found that during dehydration stress, the physical presence of ATX1 at the WRKY70 locus was diminished and that ATX1 depletion resulted from it being retained in the cytoplasm when PtdIns5P was elevated. The PHD of ATX1 and catalytically active AtMTM1 are required for the cytoplasmic localization of ATX1. The novelty of the manuscript is in the discovery of a mechanistic link between a chromatin modifying activity (ATX1) and a lipid (PtdIns5P) synthesis in a signaling pathway that ultimately results in altered expression of ATX1 dependent genes downregulated in response to dehydration stress.
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DOI：
10.1073/pnas.0510006103
发表时间：
2006-01-24
影响因子：
11.1
作者：
Begley, MJ;Taylor, GS;Dixon, JE
通讯作者：
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影响因子：
5.3
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影响因子：
6.5
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影响因子：
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影响因子：
2.9
作者：
Alvarez-Venegas, Raul;Xia, Yuannan;Avramova, Zoya
通讯作者：
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