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Abstract Repairing a damaged body part is critical for the survival of any organism. In plants, tissue damage induces rapid responses that activate defense, regeneration and wound healing. While early wound signaling mediated by phytohormones, electrical signals and reactive oxygen species is well-characterized, the mechanisms governing the final stages of wound healing remain poorly understood. Here, we show that wounding in Arabidopsis leaves induces localized cooling, likely due to evaporative water loss, accompanied by the activation of cold-responsive genes. The subsequent disappearance of localized cooling and deactivation of cold-responsive genes serve as a quantitative marker of wound healing. Based on these observations, we developed a workflow by leveraging computer vision and deep learning to monitor the dynamics of wound healing. We found that CBFs transcription factors relay injury-induced cooling signal to wound healing. Thus, our work advances our understanding of tissue repair and provides a tool to quantify wound healing in plants. 

ABSTRACT De novo root regeneration (DNRR) is a developmental process that regenerates adventitious roots from wounded tissues. Phytohormone signaling pathways involved in microbial resistance are mobilized after cutting and influence de novo root regeneration. Microbes may positively or negatively influence the development and stress responses of a plant. However, most studies on the molecular mechanisms of de novo organogenesis are performed in aseptic conditions. Thus, the potential crosstalk between organ regeneration and biotic stresses is underexplored. Here, we report the development of a versatile experimental system to study the impact of microbes on DNRR. Using this system, we found that bacteria inhibited root regeneration by activation of, but not limited to, pathogen-associated molecular pattern (PAMP)-triggered immunity. Sensing bacteria-derived flagellin 22 peptide (flg22) inhibited root regeneration by interfering with the formation of an auxin maximum at the wound site. This inhibition relies on the receptor complex that recognizes microbial patterns but may bypass the requirement of salicylic acid signaling. 

Plants can regenerate new organs from damaged or detached tissues. In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. Our work elucidates a role of SA in regulating DNRR and suggests a potential link between biotic stress and tissue regeneration.