Abstract
Stomatal closure defense and apoplastic defense are two major immunity mechanisms restricting the entry and propagation of microbe pathogens in plants. Surprisingly, activation of plant intracellular immune receptor NLR genes, while enhancing whole plant disease resistance, was sometimes linked to a defective stomatal defense in autoimmune mutants. Here we report the use of high temperature and genetic chimera to investigate the inter-dependence of stomatal and apoplastic defenses in autoimmunity. High temperature inhibits both stomatal and apoplastic defenses in the wild type, suppresses constitutive apoplastic defense responses and rescues the deficiency of stomatal closure response in autoimmune mutants. Chimeric plants have been generated to activate NLR only in guard cells or the non-guard cells. NLR activation in guard cells inhibits stomatal closure defense response in a cell autonomous manner likely through repressing ABA responses. At the same time, it leads to increased whole plant resistance accompanied by a slight increase in apoplastic defense. In addition, NLR activation in both guard and non-guard cells affects stomatal aperture and water potential. This study thus reveals that NLR activation has a differential effect on immunity in a cell type specific matter, which adds another layer of immune regulation with spatial information.
Highlights
Plant immune responses have multiple phases targeting various stages of pathogen infections
Plant immunity against foliar pathogens consists of stomatal defense to restrict the entry of pathogens and apoplastic defense to restrict the propagation of pathogens
We uncovered a previously unidentified inhibitory role of nucleotide-binding leucine-rich repeat proteins (NLR) activation in stomatal defense by using autoimmune mutants where NLR genes are activated without pathogen trigger
Summary
Plant immune responses have multiple phases targeting various stages of pathogen infections. Restriction of pathogen entry by stomatal closure upon perception of pathogen is the first line of immune responses and has been termed ‘stomatal defense’ [1,2,3,4] This stomatal defense has been known as part of the PAMP (pathogen-associated molecular patterns)-triggered immunity (PTI). ETI recognizes pathogen secreted effectors (that are intended to inhibit PTI) with plant intracellular immune receptor proteins, or resistance (R) proteins, and has a much stronger and faster immune response than that in PTI [13]. Most of these immune receptors are nucleotide-binding leucine-rich repeat proteins (NLR), some of which are indirectly involved in transcriptional control. Activation of NLR genes leads to a strong apoplastic defense and even local programmed cell death to restrict the spread of pathogens
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