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独脚金内酯在拟南芥伤口信号传导过程中调节茉莉酸依赖性转录重编程。

Strigolactones modulate jasmonate-dependent transcriptional reprogramming during wound signalling in Arabidopsis.

作者信息

Marzec Marek

机构信息

Faculty of Natural Sciences, Institute of Biology, Biotechnology and Environmental Protection, University of Silesia in Katowice, 40-032, Katowice, Poland.

出版信息

J Appl Genet. 2025 Sep 9. doi: 10.1007/s13353-025-01005-y.

Abstract

Mechanical wounding triggers rapid transcriptional and hormonal reprogramming in plants, primarily driven by jasmonate (JA) signalling. While the role of JA, ethylene, and salicylic acid in wound responses is well characterised, the contribution of strigolactones (SLs) remains largely unexplored. Here, for the first time, it was shown that SLs modulate wound-induced transcriptional dynamics in Arabidopsis thaliana. Using transcriptome profiling of wild-type (Columbia-0) and the SL biosynthesis mutant more axillary growth3 (max3), a discrete cohort of genes whose wound induction is SL-dependent was identified. These genes include core JA biosynthetic genes and several JA-responsive transcriptional repressors, indicating that SLs potentiate early JA signalling. Promoter motif and protein-protein interaction analyses revealed that SLs regulate a transcriptional module composed of AP2/ERF, WRKY, and C2H2 zinc-finger factors, which integrate JA signalling, ROS homeostasis, and tissue regeneration. Notably, many of these factors are misregulated in max3 even prior to wounding, suggesting a primed but hypo-responsive state. Presented findings suggest a model in which SLs act upstream of the JA burst, coordinating transcriptional readiness and post-injury activation. This expands the functional scope of SLs in stress response and positions them as potential modulators of hormone crosstalk during wound responses.

摘要

机械损伤会引发植物体内快速的转录和激素重编程,这主要由茉莉酸(JA)信号传导驱动。虽然JA、乙烯和水杨酸在伤口反应中的作用已得到充分表征,但独脚金内酯(SLs)的作用在很大程度上仍未被探索。在此,首次表明SLs可调节拟南芥伤口诱导的转录动态。通过对野生型(哥伦比亚-0)和SL生物合成突变体多腋生生长3(max3)进行转录组分析,鉴定出一组伤口诱导依赖于SLs的离散基因。这些基因包括核心JA生物合成基因和几个JA响应转录抑制因子,表明SLs增强了早期JA信号传导。启动子基序和蛋白质-蛋白质相互作用分析表明,SLs调节一个由AP2/ERF、WRKY和C2H2锌指因子组成的转录模块,该模块整合了JA信号传导、ROS稳态和组织再生。值得注意的是,许多这些因子在max3中甚至在受伤之前就已失调,表明处于一种预激活但反应低下的状态。目前的研究结果提出了一个模型,其中SLs在JA爆发的上游起作用,协调转录准备和损伤后激活。这扩展了SLs在应激反应中的功能范围,并将它们定位为伤口反应期间激素相互作用的潜在调节因子。

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