Translational Regulation of Metabolic Dynamics during Effector-Triggered Immunity

Yoo, Heejin; Greene, George H.; Yuan, Meng; Xu, Guoyong; Burton, D.; Liu, Lijing; Marqués, Jorge; Dong, Xinnian

doi:10.1016/j.molp.2019.09.009

Cited by 77 publications

(63 citation statements)

References 53 publications

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“…In this regard, the D111/G-patch domain-containing protein is interesting, which showed a high-confidence interaction with IBI1 and is predicted to be targeted to the nucleus ( Supplemental Table 3 ). The corresponding At5G26610 gene was recently found to be translationally regulated during effector-triggered immunity and to regulate the hypersensitive cell death response (HR) ( Yoo et al., 2020 ). In this context, it is possible that a transient interaction between the IBI1–VOZ complex and the D111/G-patch protein in the nucleus increases HR-related cell death and Hpa resistance.…”

Section: Discussionmentioning

confidence: 99%

The IBI1 Receptor of β-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

et al. 2020

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External and internal signals can prime the plant immune system for a faster and/or stronger response to pathogen attack. β-aminobutyric acid (BABA) is an endogenous stress metabolite that induces broad-spectrum disease resistance in plants. BABA perception in Arabidopsis is mediated by the aspartyl tRNA synthetase IBI1, which activates priming of multiple immune responses, including callose-associated cell wall defenses that are under control by abscisic acid (ABA). However, the immediate signaling components after BABA perception by IBI1, as well as the regulatory role of ABA therein, remain unknown. Here, we have studied the early signaling events controlling IBI1-dependent BABA-induced resistance (BABA-IR), using untargeted transcriptome and protein interaction analyses. Transcriptome analysis revealed that IBI1-dependent expression of BABA-IR against the biotrophic oomycete Hyaloperonospora arabidopsidis is associated with suppression of ABA-inducible abiotic stress genes. Protein interaction studies identified the VOZ1 and VOZ2 transcription factors (TFs) as IBI1-interacting partners, which are transcriptionally induced by ABA but suppress pathogen-induced expression of ABA-dependent genes. Furthermore, we show that VOZ TFs require nuclear localization for their contribution to BABA-IR by mediating augmented expression of callose-associated defense. Collectively, our study indicates that the IBI1-VOZ signaling module channels pathogen-induced ABA signaling toward cell wall defense while simultaneously suppressing abiotic stress-responsive genes.

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Section: Discussionmentioning

confidence: 99%

The IBI1 Receptor of β-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

et al. 2020

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“…Transcription and translation are strongly correlated during ETI 28,29 . We tested if elevated protein 35 levels of PTI signaling components results from their transcriptional induction.…”

Section: Eti Leads To Upregulation Of Pti Signaling Componentsmentioning

confidence: 99%

Mutual Potentiation of Plant Immunity by Cell-surface and Intracellular Receptors

Ngou

Ahn

Ding

et al. 2020

Preprint

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The plant immune system involves cell-surface receptors that detect intercellular pathogenderived molecules, and intracellular receptors that activate immunity upon detection of 10 pathogen-secreted effectors that act inside the plant cell. Surface receptor-mediated immunity has been extensively studied but in authentic interactions between plants and microbial pathogens, its presence impedes study of intracellular receptor-mediated immunity alone. How these two immune pathways interact is poorly understood. Here, we reveal mutual potentiation between these two recognition-dependent defense pathways. 15Recognition by surface receptors activates multiple protein kinases and NADPH oxidases, whereas intracellular receptors primarily elevate abundance of these proteins. Reciprocally, the intracellular receptor-dependent hypersensitive cell death response is strongly enhanced by activation of surface receptors. Activation of either immune system alone is insufficient to provide effective resistance against Pseudomonas syringae. Thus, immune pathways 20 activated by cell-surface and intracellular receptors mutually potentiate to activate strong defense that thwarts pathogens. By studying the activation of intracellular receptors in the absence of surface receptor-mediated immunity, we have dissected the relationship between the two distinct immune systems. These findings reshape our understanding of plant immunity and have broad implications for crop improvement. 25

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“…To further study the function of ATG4 in AvrRpt2 -induced autophagy, we did phenotypic experiments for intuitive exploration ( Figure 3 A). rps2 was used as a negative control, which fails to recognize the AvrRpt2 effector [ 20 ]. At 1 d.p.i of AvrRpt2 infection, rps2 and atg4a4b had no obvious plaques, while the leaves of npr1 and atg8a (ATG8a deletion mutant) shrunk.…”

Section: Resultsmentioning

confidence: 99%

ATG4 Mediated Psm ES4326/AvrRpt2-Induced Autophagy Dependent on Salicylic Acid in Arabidopsis Thaliana

Gong

Zhang

et al. 2020

IJMS

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Psm ES4326/AvrRpt2 (AvrRpt2) was widely used as the reaction system of hypersensitive response (HR) in Arabidopsis. The study showed that in npr1 (GFP-ATG8a), AvrRpt2 was more effective at inducing the production of autophagosome and autophagy flux than that in GFP-ATG8a. The mRNA expression of ATG1, ATG6 and ATG8a were more in npr1 during the early HR. Based on transcriptome data analysis, enhanced disease susceptibility 1 (EDS1) was up-regulated in wild-type (WT) but was not induced in atg4a4b (ATG4 deletion mutant) during AvrRpt2 infection. Compared with WT, atg4a4b had higher expression of salicylic acid glucosyltransferase 1 (SGT1) and isochorismate synthase 1 (ICS1); but less salicylic acid (SA) in normal condition and the same level of free SA during AvrRpt2 infection. These results suggested that the consumption of free SA should be occurred in atg4a4b. AvrRpt2 may trigger the activation of Toll/Interleukin-1 receptor (TIR)-nucleotide binding site (NB)-leucine rich repeat (LRR)—TIR-NB-LRR—to induce autophagy via EDS1, which was inhibited by nonexpressor of PR genes 1 (NPR1). Moreover, high expression of NPR3 in atg4a4b may accelerate the degradation of NPR1 during AvrRpt2 infection.

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Translational Regulation of Metabolic Dynamics during Effector-Triggered Immunity

Cited by 77 publications

References 53 publications

The IBI1 Receptor of β-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

The IBI1 Receptor of β-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

Mutual Potentiation of Plant Immunity by Cell-surface and Intracellular Receptors

ATG4 Mediated Psm ES4326/AvrRpt2-Induced Autophagy Dependent on Salicylic Acid in Arabidopsis Thaliana

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