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Pipecolic acid synthesis is required for systemic acquired resistance and plant-to-plant-induced immunity in barley.

J. Exp. Bot. 74, 3033-3046 (2023)
Verlagsversion DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Defense responses in plants are based on complex biochemical processes. Systemic acquired resistance (SAR) helps to fight infections by (hemi-)biotrophic pathogens. One important signaling molecule in SAR is pipecolic acid (Pip), accumulation of which is dependent on the aminotransferase ALD1 in Arabidopsis. While exogenous Pip primes defense responses in the monocotyledonous cereal crop barley (Hordeum vulgare), it is currently unclear if endogenous Pip plays a role in disease resistance in monocots. Here, we generated barley ald1 mutants using CRISPR/Cas9, and assessed their capacity to mount SAR. Endogenous Pip levels were reduced after infection of the ald1 mutant, and this altered systemic defense against the fungus Blumeria graminis f. sp. hordei. Furthermore, Hvald1 plants did not emit nonanal, one of the key volatile compounds that are normally emitted by barley plants after the activation of SAR. This resulted in the inability of neighboring plants to perceive and/or respond to airborne cues and prepare for an upcoming infection, although HvALD1 was not required in the receiver plants to mediate the response. Our results highlight the crucial role of endogenous HvALD1 and Pip for SAR, and associate Pip, in particular together with nonanal, with plant-to-plant defense propagation in the monocot crop barley.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Blumeria Graminis ; Hordeum Vulgare ; Barley ; Crispr/cas9 ; Nonanal ; Pipecolic Acid ; Plant Defense ; Plant Immunity ; Systemic Acquired Resistance ; Volatile Organic Compound; N-hydroxypipecolic Acid; Salicylic-acid; Antimicrobial Activity; Volatile Emissions; Defense; Biosynthesis; Attraction; Induction
ISSN (print) / ISBN 0022-0957
e-ISSN 1460-2431
Quellenangaben Band: 74, Heft: 10, Seiten: 3033-3046 Artikelnummer: , Supplement: ,
Verlag Oxford University Press
Verlagsort Great Clarendon St, Oxford Ox2 6dp, England
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed