4.8 Article

Elicitor-induced plant immunity relies on amino acids accumulation to delay the onset of bacterial virulence

Journal

PLANT PHYSIOLOGY
Volume 192, Issue 1, Pages 601-615

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/plphys/kiad048

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Activation of the FLS2 receptor suppresses both early infection stages' virulence and long-term growth of PstDC3000 by promoting glutamine and serine buildup in the leaf apoplast. MAMP perception in Arabidopsis induces the accumulation of free amino acids in a SA-dependent manner. Glutamine and Serine, when co-infiltrated, suppress virulence gene expression and robust infections in susceptible plants.
Activating the FLS2 receptor suppress both, the onset of PstDC3000 virulence at early infection stages, and its long-term growth, by promoting glutamine and serine buildup in the leaf apoplast. Plant immunity relies on the perception of microbe-associated molecular patterns (MAMPs) from invading microbes to induce defense responses that suppress attempted infections. It has been proposed that MAMP-triggered immunity (MTI) suppresses bacterial infections by suppressing the onset of bacterial virulence. However, the mechanisms by which plants exert this action are poorly understood. Here, we showed that MAMP perception in Arabidopsis (Arabidopsis thaliana) induces the accumulation of free amino acids in a salicylic acid (SA)-dependent manner. When co-infiltrated with Glutamine and Serine, two of the MAMP-induced highly accumulating amino acids, Pseudomonas syringae pv. tomato DC3000 expressed low levels of virulence genes and failed to produce robust infections in otherwise susceptible plants. When applied exogenously, Glutamine and Serine directly suppressed bacterial virulence and growth, bypassing MAMP perception and SA signaling. In addition, an increased level of endogenous Glutamine in the leaf apoplast of a gain-of-function mutant of Glutamine Dumper-1 rescued the partially compromised bacterial virulence- and growth-suppressing phenotype of the SA-induced deficient-2 (sid2) mutant. Our data suggest that MTI suppresses bacterial infections by delaying the onset of virulence with an excess of amino acids at the early stages of infection.

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