Abstract

Perception of microbes by plants leads to dynamic reprogramming of the transcriptome, which is essential for plant health. The appropriate amplitude of this transcriptional response can be regulated at multiple levels, including chromatin. However, the mechanisms underlying the interplay between chromatin remodeling and transcription dynamics upon activation of plant immunity remain poorly understood. Here, we present evidence that activation of plant immunity by bacteria leads to nucleosome repositioning, which correlates with altered transcription. Nucleosome remodeling follows distinct patterns of nucleosome repositioning at different loci. Using a reverse genetic screen, we identify multiple chromatin remodeling ATPases with previously undescribed roles in immunity, including EMBRYO SAC DEVELOPMENT ARREST 16, EDA16. Functional characterization of the immune-inducible chromatin remodeling ATPase EDA16 revealed a mechanism to negatively regulate immunity activation and limit changes in redox homeostasis. Our transcriptomic data combined with MNase-seq data for EDA16 functional knock-out and over-expressor mutants show that EDA16 selectively regulates a defined subset of genes involved in redox signaling through nucleosome repositioning. Thus, collectively, chromatin remodeling ATPases fine-tune immune responses and provide a previously uncharacterized mechanism of immune regulation.

Highlights

  • Plant leaf surfaces are inhabited by diverse microbial communities [1]

  • Immune signaling is tightly controlled to avoid inappropriate activation leading to severe developmental penalties

  • We explored the effect of flagellin on nucleosome remodeling at the single cell level using GFP-tagged histone H2B fluorescence recovery after photobleaching (FRAP) as a proxy for nucleosome dynamics [24]

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Summary

Introduction

Plant leaf surfaces are inhabited by diverse microbial communities [1]. Remarkably, plants are resilient to most microbial infections and disease is the exception. MTI responses include rapid production of reactive oxygen species (ROS), calcium influx, activation of mitogen-activated protein kinases (MAPKs) and differential regulation of gene expression of approximately 10 per cent of the plant genome [3,4]. These collective MTI responses are sufficient to ward off most microbes. R proteins initiate effector-triggered immunity (ETI), a strong immune response that often results in localized cell death to limit the growth and spread of the pathogen [2] Components of both MTI and ETI have been successfully employed to improve crop disease resistance [5,6]

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