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.