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甲基异噻唑啉酮污染通过改变拟南芥中的生长素运输来抑制根尖干细胞和再生。

Methylisothiazolinone pollution inhibited root stem cells and regeneration through auxin transport modification in Arabidopsis thaliana.

作者信息

You Lei, Ye Yihan, Wang Chenglin, Liu Wenqiang, Wu Shiqi, Lian Weipeng, Yang Jiahui, Lei Jinlin, Luo Xiangyin, Ye Zhengxiu, Zheng Lanlan, Zhang Yonghong, Wang Guodong, Qiu Zidong, Wang Jing, Zhang Xiaoqing, Guo Huailan, Li Chen, Liu Juan

机构信息

Laboratory of Medicinal Plant, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medicine, Hubei University of Medicine, Shiyan 442000, PR China.

Laboratory of Medicinal Plant, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medicine, Hubei University of Medicine, Shiyan 442000, PR China; School of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, China.

出版信息

J Hazard Mater. 2024 Sep 5;476:135092. doi: 10.1016/j.jhazmat.2024.135092. Epub 2024 Jul 2.

DOI:10.1016/j.jhazmat.2024.135092
PMID:
38964040
Abstract

Methylisothiazolinone (MIT) is a widely used preservative and biocide to prevent product degradation, yet its potential impact on plant growth remains poorly understood. In this study, we investigated MIT's toxic effects on Arabidopsis thaliana root growth. Exposure to MIT significantly inhibited Arabidopsis root growth, associated with reduced root meristem size and root meristem cell numbers. We explored the polar auxin transport pathway and stem cell regulation as key factors in root meristem function. Our findings demonstrated that MIT suppressed the expression of the auxin efflux carrier PIN1 and major root stem cell regulators (PLT1, PLT2, SHR, and SCR). Additionally, MIT hindered root regeneration by downregulating the quiescent center (QC) marker WOX5. Transcriptome analysis revealed MIT-induced alterations in gene expression related to oxidative stress, with physiological experiments confirming elevated reactive oxygen species (ROS) levels and increased cell death in root tips at concentrations exceeding 50 μM. In summary, this study provides critical insights into MIT's toxicity on plant root development and regeneration, primarily linked to modifications in polar auxin transport and downregulation of genes associated with root stem cell regulation.

摘要

甲基异噻唑啉酮(MIT)是一种广泛使用的防腐剂和杀菌剂,用于防止产品降解,但其对植物生长的潜在影响仍知之甚少。在本研究中,我们调查了MIT对拟南芥根生长的毒性作用。暴露于MIT会显著抑制拟南芥根的生长,这与根分生组织大小和根分生组织细胞数量减少有关。我们探讨了极性生长素运输途径和干细胞调节作为根分生组织功能的关键因素。我们的研究结果表明,MIT抑制了生长素外流载体PIN1以及主要根干细胞调节因子(PLT1、PLT2、SHR和SCR)的表达。此外,MIT通过下调静止中心(QC)标记WOX5来阻碍根再生。转录组分析揭示了MIT诱导的与氧化应激相关的基因表达变化,生理实验证实,浓度超过50μM时,根尖的活性氧(ROS)水平升高,细胞死亡增加。总之,本研究为MIT对植物根发育和再生的毒性提供了关键见解,主要与极性生长素运输的改变以及与根干细胞调节相关基因的下调有关。

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