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Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana

ABSTRACT: Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana

PROVIDER: PRJNA933934 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23423923_1.fastq.gz	Fastqsanger.gz
	SRR23423923_2.fastq.gz	Fastqsanger.gz
	SRR23423924_1.fastq.gz	Fastqsanger.gz
	SRR23423924_2.fastq.gz	Fastqsanger.gz
	SRR23423925_1.fastq.gz	Fastqsanger.gz

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Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana

Project description:Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant defense mechanism that is induced by mobile signals generated in the primarily infected leaves. Although multiple mobile SAR signals have been proposed, how these signals are perceived in the systemic leaves is unknown. Here, we show that extracellular nicotinamide adenine dinucleotide (phosphate) (eNAD(P)) accumulates in the systemic leaves and that both eNAD(P) and its receptor, the lectin receptor kinase (LecRK), LecRK-VI.2, are required in the systemic leaves for the establishment of SAR. Moreover, the mobile signal N-hydroxypipecolic acid (NHP) induces de novo NAD(P) leakage in the systemic leaves through the respiratory burst oxidase homolog RBOHF-produced reactive oxygen species (ROS). Importantly, NHP-induced systemic immunity depends on ROS, eNAD(P), and the eNAD(P) receptor complex LecRK-VI.2/ BAK1, indicating that NHP triggers SAR through the ROS-eNAD(P)-LecRK-VI.2/BAK1 signaling pathway. Our results uncovered a long-sought-after mechanism underlying the perception of mobile SAR signals in the systemic leaves

2023-10-02 | GSE225107 | GEO

Acquired MEN1 mutations mediate resistance to Menin inhibition.

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Acquired MEN1 mutations mediate resistance to Menin inhibition [CHIP-seq]

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Metabolomics analysis identifies metabolites associated with systemic acquired resistance in Arabidopsis

Project description:BACKGROUND: Systemic acquired resistance (SAR) is a plant defense response that provides long-lasting, broad-spectrum pathogen resistance to uninfected distal leaves following an initial localized infection. However, little information is available on the molecular biological basis of SAR especially in uninfected distal leaves. METHODS: Here, we used two SAR-inducing pathogen to induce SAR in Arabidopsis, and a metabolomics approach based on ultra-high-performance liquid chromatography (UPLC) and mass spectrometry (MS) technique was used to identify SAR-related metabolites in SAR-inducing pathogen infected local leaves and uninfected distal leaves. RESULTS: Multiple statistical analyses were used to identify differentially expressed metabolites. The result showed that primary metabolism and secondary metabolism were significantly altered in local leaves and distal leaves, including phenolic compounds, amino acids, nucleotides, organic acids and many other metabolites.CONCLUSIONS: The content of amino acids and phenolic compounds increased in distal leaves, suggesting their contribution to the establishment of SAR in distal leaves. In addition, 2’-hydroxy-4, 4’, 6’-trimethoxychalcone, phenylalanine and p-coumaric acid were identified as potential components which may play important roles both in basic resistance and SAR. This study provided a reference for understanding metabolic mechanism associated with SAR in Arabidopsis, which will be useful for further investigation of the molecular basis of SAR.

2020-05-14 | MTBLS1550 | MetaboLights

A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

Project description:A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

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A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

Project description:Aging is characterized by degeneration of unique tissues. However, dissecting the interconnectedness of tissue aging remains a challenge. Here, we employ a muscle-specific DNA damage model in Drosophila to reveal secreted factors that influence systemic aging in distal tissues. Utilizing this model, we uncovered a cytokine, Diedel, that when secreted from muscle or adipose can attenuate age-related intestinal tissue degeneration by promoting proliferative homeostasis of stem cells. Diedel is both necessary and sufficient to limit tissue degeneration and extend lifespan. Secreted homologs of Diedel are also found in viruses, having been acquired from host genomes. Focusing on potential mechanistic overlap between cellular aging and viral-host cell interactions and, we found that Diedel is a functionally conserved inhibitor of apoptosis and can act as a systemic rheostat to modulate cell death during aging. These results highlight a key role for secreted antagonists of apoptosis in the systemic coordination of tissue aging.

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Phosphorylation events during systemic acquired resistance in Arabidopsis

Project description:Systemic acquired resistance (SAR) is a plant defense response that provides resistance against a wide range of pathogens at the whole-plant level after a primary infection. In this study, we used a data independent acquisition (DIA) phosphoproteomics platform based on the high-resolution mass spectrometry to investigate the possible molecular mechanisms modulating protein during establishment of SAR in Arabidopsis thaliana. Then RT-qPCR and physiology assays were used to validate phosphoproteome data

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Project description:Synthesized DNA with unnatural nucleotides Synthetic Genomics

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