Epistatic chromatin remodeling during barley response to powdery mildew by ATAC-Seq

Understanding the molecular basis of plant-pathogen interactions is critical for advancing crop protection strategies. Powdery mildew, caused by the obligate fungal pathogen Blumeria hordei (Bh), is a threat to barley production worldwide. We exploited time-course ATAC-Seq of barley and derived immune mutants infected with Bh to infer chromatin accessibility influenced by the genetic interactions of mildew locus a6 (Mla6), encoding a nucleotide binding leucine-rich repeat (NLR) immune receptor, and Blufensin1 (Bln1), a basal defense regulator. Sampling at 0, 16, 20, and 32 hours after inoculation captured key pathogen developmental stages representing fungal penetration and haustorial development, respectively. Validation of the dataset was accomplished by calculating general ATAC-Seq peak metrics and comparison with paired RNA-Seq data. ATAC-Seq and RNA-Seq results were correlated, highlighting in particular chromatin-mediated epistatic interactions, demonstrating that the dataset could provide insight into regulatory chromatin architecture. These results offer a valuable dataset for dissecting transcriptional networks involved in barley immune responses.