Chromatin accessibility landscapes activated by cell-surface and intracellular immune receptors

J Exp Bot. 2021 Dec 4;72(22):7927-7941. doi: 10.1093/jxb/erab373.

Abstract

Activation of cell-surface and intracellular receptor-mediated immunity results in rapid transcriptional reprogramming that underpins disease resistance. However, the mechanisms by which co-activation of both immune systems lead to transcriptional changes are not clear. Here, we combine RNA-seq and ATAC-seq to define changes in gene expression and chromatin accessibility. Activation of cell-surface or intracellular receptor-mediated immunity, or both, increases chromatin accessibility at induced defence genes. Analysis of ATAC-seq and RNA-seq data combined with publicly available information on transcription factor DNA-binding motifs enabled comparison of individual gene regulatory networks activated by cell-surface or intracellular receptor-mediated immunity, or by both. These results and analyses reveal overlapping and conserved transcriptional regulatory mechanisms between the two immune systems.

Keywords: ATAC-seq and RNA-seq; PRR and NLR; cell surface immune receptors; chromatin accessibility; gene regulatory network; intracellular immune receptors; plant innate immunity; transcriptional regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromatin*
  • Disease Resistance
  • Gene Regulatory Networks*
  • Humans
  • Transcription Factors / genetics

Substances

  • Chromatin
  • Transcription Factors