关键词: Methylisothiazolinone Plant stem cell ROS Regeneration Root development

Mesh : Arabidopsis / drug effects metabolism genetics Indoleacetic Acids / metabolism Plant Roots / drug effects growth & development metabolism Arabidopsis Proteins / metabolism genetics Biological Transport / drug effects Reactive Oxygen Species / metabolism Gene Expression Regulation, Plant / drug effects Stem Cells / drug effects metabolism Regeneration / drug effects Oxidative Stress / drug effects Meristem / drug effects Thiazoles / toxicity

来  源:   DOI:10.1016/j.jhazmat.2024.135092

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,可防止产品降解,然而,它对植物生长的潜在影响仍然知之甚少。在这项研究中,我们研究了MIT对拟南芥根系生长的毒性作用。暴露于MIT显着抑制拟南芥根的生长,与根分生组织大小和根分生组织细胞数量减少有关。我们探索了生长素的极性转运途径和干细胞调控作为根分生组织功能的关键因素。我们的发现表明,MIT抑制了生长素外排载体PIN1和主要根干细胞调节剂(PLT1,PLT2,SHR,和SCR)。此外,MIT通过下调静止中心(QC)标记WOX5来阻碍根的再生。转录组分析显示MIT诱导的与氧化应激相关的基因表达改变,生理实验证实,浓度超过50μM时,活性氧(ROS)水平升高,根尖细胞死亡增加。总之,这项研究为麻省理工学院对植物根系发育和再生的毒性提供了重要的见解,主要与极性生长素转运的修饰和与根干细胞调控相关的基因下调有关。
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