Abstract

In eukaryotes, RNA silencing, mediated by small interfering RNAs, is an evolutionarily widespread and versatile silencing mechanism that plays an important role in various biological processes. Increasing evidences suggest that various components of RNA silencing pathway are involved in plant defense machinery against microbial pathogens in Arabidopsis thaliana. Here, we show genetic and molecular evidence that Arabidopsis SDE5 is required to generate an effective resistance against the biotrophic bacteria Pseudomonas syringae pv. tomato DC3000 and for susceptibility to the necrotrophic bacteria Erwinia caratovora pv. caratovora. SDE5, encodes a putative mRNA export factor that is indispensable for transgene silencing and the production of trans-acting siRNAs. SDE5 expression is rapidly induced by exogenous application of phytohormone salicylic acid (SA), methyl jasmonate (MeJA), phytopathogenic bacteria, and flagellin. We further report that SDE5 is involved in basal plant defense and mRNA export. Our genetic data suggests that SDE5 and Nonexpressor of PR Gene1 (NPR1) may contribute to the same SA-signaling pathway. However, SDE5 over-expressing transgenic plant exhibits reduced defense responsive phenotype after flagellin treatment. Taken together, these results support the conclusion that SDE5 contributes to plant innate immunity in Arabidopsis.

Highlights

  • Plants have evolved potent inducible immune response to multiple pathogen attacks and bacterial pathogens provide a useful example of how pathogens are encountered at various levels

  • To analyze the signaling pathway that leads to SDE5 expression, we examined pathogen-induced changes of SDE5 transcript levels in WT, as well as in mutants altered in the production of salicylic acid (SA), jasmonic acid (JA) signaling and ethylene perception following pathogen pv. tomato (Pto) DC3000 challenge

  • The Pto DC3000-induced expression of SDE5 was reduced in the pathogen-associated molecular patterns (PAMPs) receptor-defective mutants indicating a contribution of PAMP-triggered immunity (PTI) (Fig. 1B)

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Summary

Introduction

Plants have evolved potent inducible immune response to multiple pathogen attacks and bacterial pathogens provide a useful example of how pathogens are encountered at various levels. Host plants have evolved a repertoire of immune receptors, called disease resistance (R) proteins that can sense effectors and elicit effector-triggered immunity (ETI)[3, 4] Both PTI and ETI are associated with the accumulation of defense signal molecules such as salicylic acid (SA), ethylene (ET), and jasmonic acid (JA). RNA silencing is triggered by double-stranded RNA (dsRNA), processed into 21- to 24-nt short interfering (si)RNA or micro (mi)RNA by RNaseIII-like enzymes called Dicer-like proteins named DCL1–49, 10 These small RNAs guide suppression of their target gene expression at the level of transcription, RNA stability or translation. In Arabidopsis, the natural antisense transcript (NAT)-derived endogenous nat-siRNAATGB2 and AtlsiRNA-1 are induced by the bacterial pathogen Pto DC3000 carrying an effector, AvrRpt[2] These siRNAs play an important role in ETI by targeting negative regulators of the cognate R gene RPS2 signaling pathway[17, 18]. We report that SDE5 contributes to plant innate immunity in Arabidopsis via ETI pathway and suppresses PTI, while it could be induced by PAMP

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