Abstract

ABSTRACTPharmacological indications suggest that anion channel-mediated plasma membrane (PM) anion efflux is crucial in early defense signaling to induce immune responses and programmed cell death in plants. Arabidopsis SLAC1, an S-type anion channel required for stomatal closure, is involved in cryptogein-induced PM Cl− efflux to positively modulate the activation of other ion fluxes, production of reactive oxygen species and a wide range of defense responses including hypersensitive cell death in tobacco BY-2 cells. We here analyzed disease resistance against several pathogens in multiple mutants of the SLAC/SLAH channels of Arabidopsis. Resistance against a biotrophic oomycete Hyaloperonospora arabidopsidis Noco2 was significantly enhanced in the SLAC1-overexpressing plants than in the wild-type, while that against a bacteria Pseudomonas syringae was not affected significantly. Possible regulatory roles of S-type anion channels in plant immunity and disease resistance against bacterial and oomycete pathogens is discussed.

Highlights

  • In various types of mammalian cells, activation of plasma membrane (PM) Cl− channels is an early prerequisite to apoptotic events, including cell shrinkage, cytochrome c release, and programmed cell death (PCD) [1,2]

  • Recent molecular and electrophysiological studies showed that Arabidopsis SLAC1 is required for anion channel activity in the PM of guard cells and is more permeable to Cl− than malate [5], indicating that SLAC1 functions as a slow-type (S-type) anion channel located at the PM in plant cells

  • We recently revealed that Arabidopsis SLAC1 functions in the early signaling events triggered by cryptogein, a proteinaceous elicitor from an oomycete Phytophthora cryptogea, to induce PCD in tobacco BY-2 cells

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Summary

Introduction

In various types of mammalian cells, activation of plasma membrane (PM) Cl− channels is an early prerequisite to apoptotic events, including cell shrinkage, cytochrome c release, and programmed cell death (PCD) [1,2]. KEYWORDS Anion flux; SLAC/SLAH channel; disease resistance; oomycete; bacteria These data were consistent with a previous study showing that the membrane potential change triggered by flg22 as well as elf18, another typical bacterial MAMP, was not affected by anion channel inhibitors including DIDS, or by a T-DNA insertional mutation in SLAC1 or SLAH3 gene in mesophyll cells [11,12].

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