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染色质重塑是否标志着系统获得性抗性?

Does chromatin remodeling mark systemic acquired resistance?

作者信息

van den Burg Harrold A, Takken Frank L W

机构信息

Laboratory of Phytopathology, Wageningen University, Binnenhaven 5, 6709 PD Wageningen, The Netherlands.

出版信息

Trends Plant Sci. 2009 May;14(5):286-94. doi: 10.1016/j.tplants.2009.02.003.

Abstract

The recognition of plant pathogens activates local defense responses and triggers a long-lasting systemic acquired resistance (SAR) response. Activation of SAR requires the hormone salicylic acid (SA), which induces SA-responsive gene expression. Recent data link changes in gene expression to chromatin remodeling, such as histone modifications and histone replacement. Here, we propose a model in which recruitment of chromatin-modifying complexes to SA-responsive loci controls their basal and SA-induced expression. Basal repression of these loci requires the post-translational modifier SUMO (SMALL UBIQUITIN-LIKE MODIFIER). This is of particular relevance because SUMO conjugation has been shown to control the activity, assembly and disassembly of chromatin-modifying complexes to transcription complexes. Chromatin remodeling could be instrumental for priming of SA-responsive loci to enable their enhanced reactivation upon subsequent pathogen attack.

摘要

对植物病原体的识别会激活局部防御反应,并引发持久的系统获得性抗性(SAR)反应。SAR的激活需要水杨酸(SA)激素,它能诱导SA响应基因的表达。最近的数据将基因表达的变化与染色质重塑联系起来,比如组蛋白修饰和组蛋白置换。在此,我们提出一个模型,其中染色质修饰复合物被招募到SA响应位点,控制这些位点的基础表达和SA诱导的表达。这些位点的基础抑制需要翻译后修饰因子SUMO(小泛素样修饰因子)。这一点尤为重要,因为SUMO缀合已被证明可控制染色质修饰复合物到转录复合物的活性、组装和解聚。染色质重塑可能有助于SA响应位点的启动,使其在随后的病原体攻击时能够增强再激活。

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