Project description:Arabidopsis thaliana exhibits differential susceptibility to the fungal pathogen Botrytis cinerea depending on the time of day that infection occurs. We hypothesised that this is driven by teh circadian clock and that differences in the amplitude or speed of the plant defence response will underlie the difference in susceptiblity. A major component of the defence response is transcriptional reprogramming, hence we investigated whether the transcriptional response to B. cinerea infection differs following inoculation at subjective dawn or night (the points of greatest difference in susceptiblity) under constant light conditions.
Project description:Transcriptional reprogramming forms a major part of a plant's response to pathogen infection. Many individual components and pathways operating during plant defense have been identified but our knowledge of how these different components interact is still rudimentary. We have generated a high-resolution time series of gene expression profiles from a single Arabidopsis leaf during infection by the necrotrophic fungal pathogen, Botrytis cinerea. Approximately one-third of the Arabidopsis genome is differentially expressed during the first 48 hours after infection, with the majority of gene expression changes occurring before significant lesion development. We have used computational tools to obtain a detailed chronology of the defense response against B. cinerea, highlighting the times at which signaling and metabolic processes change, and identify transcription factor families operating at different times after infection. Motif enrichment and network inference predicted regulatory interactions and testing of one such prediction identified a novel role for TGA3 in defense against necrotrophic pathogens. These data provide an unprecedented level of detail about transcriptional change during a defense response and are suited to systems biology analyses to generate predictive models of the gene regulatory networks underlying the Arabidopsis response to B. cinerea.
Project description:To investigate NUP62 in the regulation of plant defense against Botrytis cinerea , we performed gene expression profiling analysis using data obtained from RNA-seq of nup62 mutant and WT arabidopsis with or without Botrytis cinerea infection.
Project description:Two samples from a larger study of the effect of Botrytis cinerea infection on gene expression in Arabidopsis thaliana. These two samples also form part of an investigation of the sequence dependancy of DNA and RNA fragmentation within ChIP-seq and RNA-seq experiments Two technical replicates from the 24 time point of a time series
Project description:Next generation sequencing was performed to identify genes changed in Arabidopsis thaliana upon Botrytis cinerea infection. The goal of the work is to find interesting genes involved in plant defense. The object is to reveal the molecular mechanism of plant defense.
Project description:In this study we show that the Arabidopsis transcription factor MYB46, previously described to regulate secondary cell wall biosynthesis in the vascular tissue of the stem, is pivotal for mediating disease susceptibility to the fungal pathogen Botrytis cinerea. We identified MYB46 by its ability to bind to a new cis element located in the 5´ promoter region of the pathogen-induced Ep5C gene which encodes a type III cell wall-bound peroxidase. We present genetic and molecular evidence indicating that MYB46 modulates the magnitude of Ep5C gene induction following pathogenic insults. Moreover, we demonstrate that different myb46 knock-down mutant plants exhibit increased disease resistance to B. cinerea, a phenotype that is accompanied by selective transcriptional reprogramming of a set of genes encoding cell wall proteins and enzymes, of which extracellular type III peroxidases are conspicuous. In essence our results substantiates that defense-related signaling pathways and cell wall integrity are interconnected, and MYB46 likely functions as a disease susceptibility modulator to B. cinerea through the integration of cell wall remodeling and downstream activation of secondary lines of defense.
