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<p>Acetic acid is a cost-effective and eco-friendly metabolite that enhances plant tolerance to diverse abiotic stresses. Yet, its regulatory role in plant growth and the associated mechanisms remain less understood. This study aimed to characterize the effect of acetic acid on perennial ryegrass growth and its underlying mechanisms. Concentration screening identified 2&#xa0;mM as the optimal concentration that significantly inhibited ryegrass growth under both soil and hydroponic conditions, as evidenced by reduced plant height, biomass, total root length, and root tip numbers. Paraffin sectioning with Safranin O-Fast Green staining revealed that acetic acid promoted root cell wall lignification and suppressed root tip cell expansion, leading to a reduced root cap length, cortex thickness, and stele diameter. Transcriptome sequencing identified 760 differentially expressed genes (DEGs) enriched in phenylpropanoid biosynthesis, nitrogen metabolism, and plant hormone signal transduction pathways. Key DEGs included down-regulated gibberellin (GA) oxidase genes (e.g., <i>GA20OX1s</i>, <i>GA2OX3s</i>, and <i>GA2OX6</i>), auxin transporter genes (e.g., <i>PIN2</i>, <i>PIN5B</i>, and <i>ABCB15</i>), and 19 out of 20 differentially expressed expansin genes, which are consistent with reduced endogenous GA₃ and indole-3-acetic acid (IAA) levels in acetic acid-treated plants. Exogenous application of GA₃ or IAA alleviated acetic acid-induced growth inhibition, while GA or IAA biosynthesis inhibitors (CCC, L-K) mimicked the growth-retarding effect of acetic acid, confirming GA and IAA metabolism mediates acetic acid-regulated growth. Notably, acetic acid’s growth-inhibitory effect was conserved across monocot (wheat) and dicot (tobacco, cotton) species. Collectively, acetic acid inhibits plant growth by promoting root cell wall lignification, down-regulating growth-related genes, and disrupting GA/IAA homeostasis.</p>

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Acetic Acid Suppresses Perennial Ryegrass Growth In Vitro by Disrupting Gibberellin and Auxin Homeostasis and Restricting Cell Expansion

  • 期刊论文

  • 发表日期：

    2026年6月26日

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  • Hao Guan,
  • Caiyi Xie,
  • Weiyu Jia,
  • Ruiting Ouyang,
  • Yuhan Xia,
  • Yuhan Fu,
  • Yi Man,
  • Huaiyang Hou,
  • Yingjun Chi,
  • Bin Xu,
  • Jing Zhang

摘要

Acetic acid is a cost-effective and eco-friendly metabolite that enhances plant tolerance to diverse abiotic stresses. Yet, its regulatory role in plant growth and the associated mechanisms remain less understood. This study aimed to characterize the effect of acetic acid on perennial ryegrass growth and its underlying mechanisms. Concentration screening identified 2 mM as the optimal concentration that significantly inhibited ryegrass growth under both soil and hydroponic conditions, as evidenced by reduced plant height, biomass, total root length, and root tip numbers. Paraffin sectioning with Safranin O-Fast Green staining revealed that acetic acid promoted root cell wall lignification and suppressed root tip cell expansion, leading to a reduced root cap length, cortex thickness, and stele diameter. Transcriptome sequencing identified 760 differentially expressed genes (DEGs) enriched in phenylpropanoid biosynthesis, nitrogen metabolism, and plant hormone signal transduction pathways. Key DEGs included down-regulated gibberellin (GA) oxidase genes (e.g., GA20OX1s, GA2OX3s, and GA2OX6), auxin transporter genes (e.g., PIN2, PIN5B, and ABCB15), and 19 out of 20 differentially expressed expansin genes, which are consistent with reduced endogenous GA₃ and indole-3-acetic acid (IAA) levels in acetic acid-treated plants. Exogenous application of GA₃ or IAA alleviated acetic acid-induced growth inhibition, while GA or IAA biosynthesis inhibitors (CCC, L-K) mimicked the growth-retarding effect of acetic acid, confirming GA and IAA metabolism mediates acetic acid-regulated growth. Notably, acetic acid’s growth-inhibitory effect was conserved across monocot (wheat) and dicot (tobacco, cotton) species. Collectively, acetic acid inhibits plant growth by promoting root cell wall lignification, down-regulating growth-related genes, and disrupting GA/IAA homeostasis.