School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68588 USA.
Epigenetics Chromatin. 2016 Feb 24;9:8. doi: 10.1186/s13072-016-0057-5. eCollection 2016.
Plant genes that provide a different response to a similar dehydration stress illustrate the concept of transcriptional 'dehydration stress memory'. Pre-exposing a plant to a biotic stress or a stress-signaling hormone may increase transcription from response genes in a future stress, a phenomenon known as 'gene priming'. Although known that primed transcription is preceded by accumulation of H3K4me3 marks at primed genes, what mechanism provides for their appearance before the transcription was unclear. How augmented transcription is achieved, whether/how the two memory phenomena are connected at the transcriptional level, and whether similar molecular and/or epigenetic mechanisms regulate them are fundamental questions about the molecular mechanisms regulating gene expression.
Although the stress hormone jasmonic acid (JA) was unable to induce transcription of tested dehydration stress response genes, it strongly potentiated transcription from specific ABA-dependent 'memory' genes. We elucidate the molecular mechanism causing their priming, demonstrate that stalled RNA polymerase II and H3K4me3 accumulate as epigenetic marks at the JA-primed ABA-dependent genes before actual transcription, and describe how these events occur mechanistically. The transcription factor MYC2 binds to the genes in response to both dehydration stress and to JA and determines the specificity of the priming. The MEDIATOR subunit MED25 links JA-priming with dehydration stress response pathways at the transcriptional level. Possible biological relevance of primed enhanced transcription from the specific memory genes is discussed.
The biotic stress hormone JA potentiated transcription from a specific subset of ABA-response genes, revealing a novel aspect of the JA- and ABA-signaling pathways' interactions. H3K4me3 functions as an epigenetic mark at JA-primed dehydration stress response genes before transcription. We emphasize that histone and epigenetic marks are not synonymous and argue that distinguishing between them is important for understanding the role of chromatin marks in genes' transcriptional performance. JA-priming, specifically of dehydration stress memory genes encoding cell/membrane protective functions, suggests it is an adaptational response to two different environmental stresses.
在相似的脱水胁迫下表现出不同响应的植物基因，阐明了转录“脱水胁迫记忆”的概念。预先暴露于生物胁迫或应激信号激素的植物，可能会在未来的应激中增加响应基因的转录，这种现象被称为“基因启动”。尽管已知启动转录之前，启动基因上会积累 H3K4me3 标记，但在转录之前，这些标记是如何出现的尚不清楚。增强转录是如何实现的，这两种记忆现象在转录水平上是如何联系的，以及是否有类似的分子和/或表观遗传机制来调节它们，这些都是关于调节基因表达的分子机制的基本问题。
尽管应激激素茉莉酸（JA）不能诱导测试的脱水胁迫响应基因的转录，但它强烈增强了特定 ABA 依赖性“记忆”基因的转录。我们阐明了导致其启动的分子机制，证明了停滞的 RNA 聚合酶 II 和 H3K4me3 在实际转录之前作为表观遗传标记积累在 JA 启动的 ABA 依赖性基因上，并描述了这些事件是如何发生的。转录因子 MYC2 响应于脱水胁迫和 JA 与 MED25 结合，将 MED25 连接到基因上，决定了启动的特异性。JA 启动与转录水平上的脱水胁迫响应途径的 MED25 连接。讨论了特定记忆基因增强转录的潜在生物学相关性。
生物胁迫激素 JA 增强了特定 ABA 响应基因的转录，揭示了 JA 和 ABA 信号通路相互作用的一个新方面。H3K4me3 作为 JA 启动的脱水胁迫响应基因转录前的表观遗传标记。我们强调，组蛋白和表观遗传标记不是同义词，并且区分它们对于理解染色质标记在基因转录性能中的作用很重要。JA 启动，特别是编码细胞/膜保护功能的脱水胁迫记忆基因的启动，表明这是对两种不同环境胁迫的适应性反应。
