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

## TL;DR

This study shows that strigolactones help regulate plant wound responses by influencing jasmonate signaling and gene activity in Arabidopsis.

## Contribution

The study is the first to demonstrate that strigolactones modulate wound-induced transcriptional dynamics in plants.

## Key findings

- Strigolactones potentiate early jasmonate signaling by regulating key biosynthetic genes and transcriptional repressors.
- SLs influence a transcriptional module involving AP2/ERF, WRKY, and C2H2 zinc-finger factors linked to wound responses.
- The SL biosynthesis mutant max3 shows misregulation of wound-related genes even before injury, indicating a primed state.

## 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.

The online version contains supplementary material available at 10.1007/s13353-025-01005-y.