Cysteine signaling in plant pathogen response

Abstract The amino acid cysteine is the precursor for a wide range of sulfur-containing functional molecules in plants, including enzyme cofactors and defense compounds. Due to its redox active thiol group cysteine is highly reactive. Synthesis and degradation pathways are present in several subcellular compartments to adjust the intracellular cysteine concentration. However, stress conditions can lead to a transient increase in local cysteine levels. Here we investigate links between cysteine homeostasis and metabolic signaling in Arabidopsis thaliana. The systemic proteome response to cysteine feeding strongly suggests that Arabidopsis seedlings interpret accumulation of cysteine above a certain threshold as a signal for a biotic threat. Cysteine supplementation of Arabidopsis plants via the roots increases their resistance to the hemibiotrophic bacterium Pseudomonas syringae confirming the protective function of the cysteine induced defense pathways. Analysis of mutant plants reveals that the balance of cysteine synthesis between the cytosol and organelles is crucial during Arabidopsis immune response to Pseudomonas syringae. The induction profile of pathogen responsive proteins by cysteine provides insight into potential modes of action. Our results highlight the role of cysteine as a metabolic signal in the plant immune response and add evidence to the emerging concept of intracellular organelles as important players in plant stress signaling. Competing Interest Statement The authors have declared no competing interest. Footnotes For the revised version of our manuscript we performed additional experiments to validate some of the findings from proteomics. We added a new supplementary figure (Suppl. Fig. S3) to present the results of all validation experiments. In order to facilitate a comparison between the proteomics datasets we also introduced a new supplementary dataset (Suppl. Dataset S3), with filtering options for common proteome responses to cysteine feeding and pathogen attack as well as for the overlap between the two timepoints in pathogen response (24 hpi and 48 hpi). We also added more details on statistics and improved the clarity of our line of arguments in the results and discussion sections.