Endogenous salicylic acid suppresses de novo root regeneration from leaf explants

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 o...

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Published in:PLoS genetics 2023-03, Vol.19 (3), p.e1010636-e1010636
Main Authors: Tran, Sorrel, Ison, Madalene, Ferreira Dias, Nathália Cássia, Ortega, Maria Andrea, Chen, Yun-Fan Stephanie, Peper, Alan, Hu, Lanxi, Xu, Dawei, Mozaffari, Khadijeh, Severns, Paul M, Yao, Yao, Tsai, Chung-Jui, Teixeira, Paulo José Pereira Lima, Yang, Li
Format: Article
Language:English
Subjects:
Analysis
Arabidopsis - metabolism
Arabidopsis Proteins - metabolism
Auxin
Biology and Life Sciences
Biosynthesis
Defense industry
Dosage and administration
Environmental aspects
Experiments
Explants
Foliage plants
Gene Expression Regulation, Plant
Genes
Genetic aspects
Growth
Instrument industry
Leaves
Organogenesis
Pathogens
Phenols
Plant Growth Regulators - metabolism
Plant Growth Regulators - pharmacology
Plant hormones
Plant Leaves - metabolism
Plant Roots - genetics
Plant Roots - metabolism
Research and Analysis Methods
Roots (Botany)
Salicylic acid
Salicylic Acid - metabolism
Transcription factors
Wounding
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Summary: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.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1010636