Project description:We determined on a genome-wide scale the flg22-induced in vivo DNA-binding dynamics of three of the most prominent WRKY factors, WRKY18, WRKY40 and WRKY33. The three WRKY factors each bound to more than 1000 gene loci predominantly at W-box elements, the known WRKY binding motif. Transcriptional analysis also revealed that WRKY18 and WRKY40 function redundantly as negative regulators of flg22-induced genes.
Project description:We determined on a genome-wide scale the flg22-induced in vivo DNA-binding dynamics of three of the most prominent WRKY factors, WRKY18, WRKY40 and WRKY33. The three WRKY factors each bound to more than 1000 gene loci predominantly at W-box elements, the known WRKY binding motif. Transcriptional analysis also revealed that WRKY18 and WRKY40 function redundantly as negative regulators of flg22-induced genes.
Project description:During microbe-associated molecular pattern (MAMP)-triggered immunity (MTI) more than 5000 Arabidopsis genes are significantly altered in their expression and the question arises, how such an enormous reprogramming of the transcriptome can be regulated in a safe and robust manner? For the WRKY transcription factors, which are important regulators not only of this defense response, it appears that they act in a complex regulatory sub-network rather than in a linear fashion, which is much more vulnerable to gene function loss either by pathogen-derived effectors or by mutations. In this study we employed RNA-seq, mass spectrometry and ChIP-seq to find evidence for and uncover principles and characteristics of this network.
Project description:During microbe-associated molecular pattern (MAMP)-triggered immunity (MTI) more than 5000 Arabidopsis genes are significantly altered in their expression and the question arises, how such an enormous reprogramming of the transcriptome can be regulated in a safe and robust manner? For the WRKY transcription factors, which are important regulators not only of this defense response, it appears that they act in a complex regulatory sub-network rather than in a linear fashion, which is much more vulnerable to gene function loss either by pathogen-derived effectors or by mutations. In this study we employed RNA-seq, mass spectrometry and ChIP-seq to find evidence for and uncover principles and characteristics of this network.
Project description:Phytosulfokine (PSK) is a plant growth-promoting peptide hormone that is perceived by its cell surface receptors PSKR1 and PSKR2 in Arabidopsis. Plants lacking the PSK receptors show phenotypes consistent with PSK signaling repressing some plant defenses. To gain further insight into the PSK signaling mechanism, comprehensive transcriptional profiling of Arabidopsis treated with PSK was performed, and the effects of PSK treatment on plant defense readouts were monitored. Our study indicates that PSK's major effect is to downregulate defense-related genes; it has a more modest effect on the induction of growth-related genes. WRKY transcription factors (TFs) emerged as key regulators of PSK-responsive genes, sharing commonality with a pathogen-associated molecular pattern (PAMP) responses, flagellin 22 (flg22), but exhibiting opposite regulatory directions. These PSK-induced transcriptional changes were accompanied by biochemical and physiological changes that reduced PAMP responses, notably mitogen-activated protein kinase (MPK) phosphorylation (previously implicated in WRKY activation) and the cell wall modification of callose deposition. Comparison with previous studies using other growth stimuli (the sulfated plant peptide containing sulfated tyrosine [PSY] and Pseudomonas simiae strain WCS417) also reveals WRKY TFs' overrepresentations in these pathways, suggesting a possible shared mechanism involving WRKY TFs for plant growth-defense trade-off.