ArticleNature plants2025
A root-based N-hydroxypipecolic acid standby circuit to direct immunity and growth of Arabidopsis shoots.
Article in Nature plants, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- SARD1 and CBP60g redundantly regulate N-hydroxypipecolic acid- and salicylic acid-dependent systemic immunity but are dispensable for the activation of indolic defense metabolism.The Plant journal : for cell and molecular biology · 2026Article
- Systemic acquired resistance: an emerging role for jasmonates in local signal biogenesis, translocation and distal signal decoding.The New phytologist · 2026Review
- Identification of candidate genes associated with major QTL controlling Vertcillium wilt resistance in cotton (Gossypium hirsutum L.).TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2026Article
- The plant holobiont: integrating molecular priming and ecological legacies for climate-adaptive immunity.Essays in biochemistry · 2026Review
- Back to the roots: Cannabis sativa L. root metabolism, microbiomes, and biotechnological potential.Applied microbiology and biotechnology · 2026Review
- Flavin-Containing Monooxygenase 1 Gene Mediates Resistance toPlants (Basel, Switzerland) · 2026Article
- N-hydroxy-pipecolic acid-mediated signal transduction and resistance requires DAWDLE.Plant physiology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Soil-borne microorganisms can systemically affect shoot resistance to pathogens relying on jasmonic acid and/or salicylic acid. However, the emanating root triggers in these scenarios remain elusive. Here we identify an N-hydroxypipecolic-acid-(NHP-)directed, salicylic-acid-related mechanism of root-triggered systemic resistance in Arabidopsis, which uses components of systemic acquired resistance known in leaves. However, in contrast to the inductive nature of systemic acquired resistance, FLAVIN-DEPENDENT MONOOXYGENASE 1 (FMO1) continuously synthesizes NHP in roots, while the glucosyltransferase UGT76B1 concomitantly conjugates and immobilizes NHP. Physical grafting experiments and tissue-specific knockouts revealed that the loss of UGT76B1 in roots leads to enhanced NHP release, initiating shoot responses. This counteracting standby FMO1/UGT76B1 circuit is specifically and sensitively modulated by root-associated microorganisms. Endophytic and (hemi)biotrophic fungi induce UGT76B1 degradation and FMO1 expression, resulting in varying levels of NHP being released to the shoot, where this root signal differently modulates defence and growth.
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