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<p>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 <i>Arabidopsis thaliana</i>. Using transcriptome profiling of wild-type (Columbia-0) and the SL biosynthesis mutant <i>more axillary growth3</i> (<i>max3</i>), 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 <i>max3</i> 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月9日

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  • Marek Marzec

摘要

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.