University of Nebraska Center for Biotechnology and Center for Plant Science Innovation, 1901 Vine Street, Lincoln, NE 68588, USA.
Plant J. 2011 Jun;66(5):735-44. doi: 10.1111/j.1365-313X.2011.04534.x. Epub 2011 Apr 1.
Emerging evidence suggests that the molecular mechanisms driving the responses of plants to environmental stresses are associated with specific chromatin modifications. Here, we demonstrate that the Arabidopsis trithorax-like factor ATX1, which trimethylates histone H3 at lysine 4 (H3K4me3), is involved in dehydration stress signaling in both abscisic acid (ABA)-dependent and ABA-independent pathways. The loss of function of ATX1 results in decreased germination rates, larger stomatal apertures, more rapid transpiration and decreased tolerance to dehydration stress in atx1 plants. This deficiency is caused in part by reduced ABA biosynthesis in atx1 plants resulting from decreased transcript levels from NCED3, which encodes a key enzyme controlling ABA production. Dehydration stress increased ATX1 binding to NCED3, and ATX1 was required for the increased levels of NCED3 transcripts and nucleosomal H3K4me3 that occurred during dehydration stress. Mechanistically, ATX1 affected the quantity of RNA polymerase II bound to NCED3. By upregulating NCED3 transcription and ABA production, ATX1 influenced ABA-regulated pathways and genes. ATX1 also affected the expression of ABA-independent genes, implicating ATX1 in diverse dehydration stress-response mechanisms in Arabidopsis.
新出现的证据表明，驱动植物对环境胁迫做出反应的分子机制与特定的染色质修饰有关。在这里，我们证明拟南芥 trithorax 样因子 ATX1 会使组蛋白 H3 在赖氨酸 4 位三甲基化（H3K4me3），其参与到依赖和不依赖脱落酸（ABA）的两条脱水胁迫信号通路中。ATX1 的功能丧失导致发芽率降低、气孔开度更大、蒸腾速率更快，并且 ATX1 植株对脱水胁迫的耐受性降低。这种缺陷部分是由于 atx1 植物中 NCED3 的转录水平降低，导致 ABA 生物合成减少所致，NCED3 编码控制 ABA 产生的关键酶。脱水胁迫增加了 ATX1 与 NCED3 的结合，而 ATX1 是 NCED3 转录本和核小体 H3K4me3 在脱水胁迫过程中增加所必需的。在机制上，ATX1 影响 RNA 聚合酶Ⅱ与 NCED3 的结合量。通过上调 NCED3 转录和 ABA 产生，ATX1 影响了 ABA 调节的途径和基因。ATX1 还影响了 ABA 不依赖基因的表达，表明 ATX1 参与了拟南芥中多种脱水胁迫反应机制。
