ArticlePLoS genetics2023
Endogenous salicylic acid suppresses de novo root regeneration from leaf explants.
Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Stem cell activity is linked to a transient acquisition of pluripotency during callus proliferation.Nature communications · 2026Article
- EnhancedPlants (Basel, Switzerland) · 2025Article
- Proline transporters balance the salicylic acid-mediated trade-off between regeneration and immunity in plants.bioRxiv : the preprint server for biology · 2025Article
- Regeneration and defense: unveiling the molecular interplay in plants.The New phytologist · 2025Review
- Evaporative cooling signals for wound healing in plants.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomic and hormonal dynamics in relation to adventitious rooting of two parentalFrontiers in plant science · 2025Article
- Altering cold-regulated gene expression decouples the salicylic acid-growth trade-off in Arabidopsis.The Plant cell · 2024Article
- Plant regeneration in the new era: from molecular mechanisms to biotechnology applications.Science China. Life sciences · 2024Review
- Article
- Microbial pattern recognition suppresses de novo organogenesis.Development (Cambridge, England) · 2023Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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