Prof. University of California, San Diego La Jolla, California
Body of Abstract: In plants, epidermal guard cells integrate and respond to numerous environmental signals to control the aperture of the stomatal pore thereby limiting water loss and regulating gas exchange. Chromatin structure controls access of transcription factors to the genome, but whether large-scale chromatin remodelling occurs in guard cells during stomatal movements is unknown. We examined how the guard cell epigenome responds to the stress hormone abscisic acid (ABA) and to changes in CO2 concentration, two signals of importance to stomatal function and plant biology. We developed cell-sorting strategies to isolate guard cell nuclei from soil-grown Arabidopsis thaliana and then performed ATAC-Seq to measure genome-wide chromatin accessibility. Our analysis identified many putative guard specific regulatory elements in the genome. We then examined ABA-induced chromatin remodelling in seedlings, and in mesophyll and guard cells from mature plants. We found that ABA triggers genome-wide and persistent changes to chromatin accessibility, with ABA inducing chromatin opening at the promoters of ABA-induced genes and chromatin closing near ABA-repressed genes. DNA motif analysis uncovered binding sites for distinct transcription factors enriched in ABA-induced and ABA-repressed chromatin. By profiling chromatin accessibility in mutant guard cells, we discovered that specific transcription factors are required for ABA-triggered epigenome reprogramming. We also uncovered that ABA and CO2 induce distinct programs of chromatin remodeling in guard cells. We propose a model in which closed chromatin states in the absence of stress and ABA-induced chromatin remodeling in response to stress promote abiotic stress resistance.