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茉莉酸相关拟南芥基因对反复脱水胁迫的记忆反应。

Memory responses of jasmonic acid-associated Arabidopsis genes to a repeated dehydration stress.

作者信息

Liu Ning, Staswick Paul E, Avramova Zoya

机构信息

School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA.

Department of Agronomy and Horticulture, University of Nebraska-Lincoln, Lincoln, NE, 68588, USA.

出版信息

Plant Cell Environ. 2016 Nov;39(11):2515-2529. doi: 10.1111/pce.12806. Epub 2016 Sep 30.

Abstract

Dehydration stress activates numerous genes co-regulated by diverse signaling pathways. Upon repeated exposures, however, a subset of these genes does not respond maintaining instead transcription at their initial pre-stressed levels ('revised-response' genes). Most of these genes are involved in jasmonic acid (JA) biosynthesis, JA-signaling and JA-mediated stress responses. How these JA-associated genes are regulated to provide different responses to similar dehydration stresses is an enigma. Here, we investigate molecular mechanisms that contribute to this transcriptional behavior. The memory-mechanism is stress-specific: one exposure to dehydration stress or to abscisic acid (ABA) is required to prevent transcription in the second. Both ABA-mediated and JA-mediated pathways are critical for the activation of these genes, but the two signaling pathways interact differently during a single or multiple encounters with dehydration stress. Synthesis of JA during the first (S1) but not the second dehydration stress (S2) accounts for the altered transcriptional responses. We propose a model for these memory responses, wherein lack of MYC2 and of JA synthesis in S2 is responsible for the lack of expression of downstream genes. The similar length of the memory displayed by different memory-type genes suggests biological relevance for transcriptional memory as a gene-regulating mechanism during recurring bouts of drought.

摘要

脱水胁迫会激活众多由不同信号通路共同调控的基因。然而,在反复暴露后,这些基因中的一部分不会产生反应,而是维持其初始应激前水平的转录(“修正反应”基因)。这些基因中的大多数参与茉莉酸(JA)生物合成、JA信号传导和JA介导的应激反应。这些与JA相关的基因是如何被调控以对相似的脱水胁迫产生不同反应的,仍是一个谜。在此,我们研究了促成这种转录行为的分子机制。记忆机制具有应激特异性:需要一次脱水胁迫或脱落酸(ABA)暴露,才能阻止第二次暴露时的转录。ABA介导的途径和JA介导的途径对于这些基因的激活都至关重要,但在单次或多次脱水胁迫过程中,这两条信号通路的相互作用方式不同。第一次脱水胁迫(S1)而非第二次脱水胁迫(S2)期间JA的合成导致了转录反应的改变。我们提出了一个针对这些记忆反应的模型,其中S2中MYC2和JA合成的缺失导致了下游基因表达的缺失。不同记忆类型基因所显示的相似记忆时长表明,转录记忆作为干旱反复发生期间的一种基因调控机制具有生物学意义。

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