Abstract

Phytopathogens, such as biotrophs, hemibiotrophs and necrotrophs, pose serious stress on the development of their host plants, compromising their yields. Plants are in constant interaction with such phytopathogens and hence are vulnerable to their attack. In order to counter these attacks, plants need to develop immunity against them. Consequently, plants have developed strategies of recognizing and countering pathogenesis through pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Pathogen perception and surveillance is mediated through receptor proteins that trigger signal transduction, initiated in the cytoplasm or at the plasma membrane (PM) surfaces. Plant hosts possess microbe-associated molecular patterns (P/MAMPs), which trigger a complex set of mechanisms through the pattern recognition receptors (PRRs) and resistance (R) genes. These interactions lead to the stimulation of cytoplasmic kinases by many phosphorylating proteins that may also be transcription factors. Furthermore, phytohormones, such as salicylic acid, jasmonic acid and ethylene, are also effective in triggering defense responses. Closure of stomata, limiting the transfer of nutrients through apoplast and symplastic movements, production of antimicrobial compounds, programmed cell death (PCD) are some of the primary defense-related mechanisms. The current article highlights the molecular processes involved in plant innate immunity (PII) and discusses the most recent and plausible scientific interventions that could be useful in augmenting PII.

Highlights

  • The current review provides an overview of the existing state of knowledge in the area of plant innate immunity (PII) and updates on the recent information that have been added to the various aspects of PII currently discussed

  • This study indicated that intracellular distribution and abundance of StEXPAs and HRGPs can be differentially regulated, which depends on different types of PVYNTN –potato plant interactions and further confirmed the involvement of apoplast and symplast activation as a defense response mechanism [132]

  • Plant hosts possess microbe-associated molecular patterns (P/MAMPs), which trigger a complex set of mechanisms through the pattern recognition receptors (PRRs) and resistance (R) genes

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. As a result of pathogen attack, the plants recognize that their peptides are continuously synthesized These are released into the extracellular space, including plant apoplast, from their normal location due to damage (trauma), and these molecules are referred to as damage-associated molecular patterns (DAMPs) [12,13,14]. EATP is found to induce typical innate immune responses that include cytosolic Ca2+ influx, MAPK activation, and induction of some dense-associated genes that are involved in the biosynthesis of JA and ethylene [21]. It is unclear yet whether it contributes to resistance to pathogens. The plants recruit many cell-surface and intracellular immune receptors to perceive a variety of immunogenic signals associated with pathogen infection and followed by the activation of defensive signaling cascades [23]

Bacteria
PTI—ETI Mutualism
Brassinosteroids
Ethylene
Abscisic Acid
Protein Kinase Signaling Impacts Chromatin Reprogramming in Plant Defense
Chromatin Structure and Modifications
Conclusions and Recommendations
Full Text
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