Silencing and Innate Immunity in Plant Defense Against Viral and Non-Viral Pathogens

Abstract

The frontline of plant defense against non-viral pathogens such as bacteria, fungi and oomycetes is provided by transmembrane pattern recognition receptors that detect conserved pathogen-associated molecular patterns (PAMPs), leading to pattern-triggered immunity (PTI). To counteract this innate defense, pathogens deploy effector proteins with a primary function to suppress PTI. In specific cases, plants have evolved intracellular resistance (R) proteins detecting isolate-specific pathogen effectors, leading to effector-triggered immunity (ETI), an amplified version of PTI, often associated with hypersensitive response (HR) and programmed cell death (PCD). In the case of plant viruses, no conserved PAMP was identified so far and the primary plant defense is thought to be based mainly on RNA silencing, an evolutionary conserved, sequence-specific mechanism that regulates gene expression and chromatin states and represses invasive nucleic acids such as transposons. Endogenous silencing pathways generate 21-24 nt small (s)RNAs, miRNAs and short interfering (si)RNAs, that repress genes post-transcriptionally and/or transcriptionally. Four distinct Dicer-like (DCL) proteins, which normally produce endogenous miRNAs and siRNAs, all contribute to the biogenesis of viral siRNAs in infected plants. Growing evidence indicates that RNA silencing also contributes to plant defense against non-viral pathogens. Conversely, PTI-based innate responses may contribute to antiviral defense. Intracellular R proteins of the same NB-LRR family are able to recognize both non-viral effectors and avirulence (Avr) proteins of RNA viruses, and, as a result, trigger HR and PCD in virus-resistant hosts. In some cases, viral Avr proteins also function as silencing suppressors. We hypothesize that RNA silencing and innate immunity (PTI and ETI) function in concert to fight plant viruses. Viruses counteract this dual defense by effectors that suppress both PTI-/ETI-based innate responses and RNA silencing to establish successful infection.

Modulation of host plant immunity by Tobamovirus proteins

“…The chronology of the events proposed is in agreement with the zig-zag model of the plant-pathogen interaction which is represented at the base of Figure 2 (Jones and Dangl, 2006;Zvereva and Pooggin, 2012). In this, the deployment of consecutive rounds of defense and counter-defense will determine whether infection occurs or not.…”

Computational Tools for Investigating RNA-Protein Interaction Partners

“…RNA-protein interactions (RPIs) also play important roles in human health and diseases [4], as well as in viral replication [5], and pathogen resistance in plants [6]. Even though the human genome contains more than 400 known or predicted RBPs [7,8], the structures of RNA-protein complexes and the roles of RPIs in post-transcriptional regulatory networks [1,9], are much less well characterized than the DNA-protein complexes involved in transcriptional regulation.…”

"HoneySweet" Plum—A Valuable Genetically Engineered Fruit-Tree Cultivar

“…"HoneySweet" plum has proven to be highly resistant to PPV [7] and this high level of resistance has remained stable in European field tests for over 15 years under high PPV infection pressure [8]. Resistance in "HoneySweet" is based on gene silencing or RNA interference (RNAi) which is a natural virus defense system in plants [9]. RNAi in "HoneySweet" produces a high level of resistance that prevents systemic virus infection [10].…”