Hypersensitivity and its Mechanism

Introduction

The HR is a localized induced cell defense in the host plant

at the site of infection by a pathogen.

HR responsible for limiting the growth of the pathogen by this way it

provide resistance to host against pathogen.

Most Hypersensitive response involve only single cell or very few cells.

Contd..

Whenever the virulent pathogen artificially injected to non host plant or

resistant plant and when avirulent strain into susceptible host plant it

induce hypersensitive response.

The HR is the culmination of the plant defense responses initiated by the

recognition of specific pathogen signal molecules, known as elicitors by plant.

The HR occur only in specific host-pathogen combination in which the host

and pathogen are incompatible.

Its occur only in Vertical resistance.

R gene and Pattern Recognition Receptor plant (Extra cellular /intra cellular)

Mechan i sm

PAMP / MAMP /elicitor of

pathogen

T3SS of Bacteria

Compatible interaction between R gene product and Elicitor activates a

cascade of biochemical reaction and activate defense related compound.

Phase 1. The activation of R genes triggers an ion flux (efflux of hydroxide andpotassium, and influx of calcium and hydrogen ions) {Orlandi et al. 1992}

Phase 2. These generate an oxidative burst by producing reactive oxygenspecies (ROS).

These compounds induce lipid peroxidation hence lipid damage, whichdegrade cellular membrane function. {Baker et al. 1993}

That results in the death of affected cells and the formation of local lesions.

This event increase biosynthesis of salicylic acid (SA), jasmonic acid (JA)

and ethylene (ET) which leads to long-lasting systemic acquired resistance (SAR).

JA-dependent defense responses activated by necrotrophic pathogens,

and SA-dependent responses triggered by biotrophic pathogens .

Conclusion of HR

Depolarization of the membrane

Electrolyte leakage

Loss of selective membrane permeability

Apposition of material to the cell wall

Increased cytoplasmic streaming

Translocation of the nucleus to infection site

Callose deposition and papillae formation

Condensation of Nucleoplasm and cytoplasm

Disintegration of Cytoskeleton

Cleavage of nuclear DNA

In the absence of pathogen challenge, NPR1 (non-expresser of pathogenesis-related genes 1) is retained in the cytoplasm as an oligomer through redox-sensitive intermolecular di-sulphide bonds.

After induction, these di-sulphide bonds are reduced, releasing NPR1 monomers into the nucleus, where NPR1 acts as a cofactor for transcription factors to induce defense related genes.

Two receptors for salicylic acid NPR3 and NPR4 in cytoplasm.

NPR3 has high affinity with SA as compared to NPR4.

Why cell death occur only at the site of Infection

SA + NPR4 = di-sulphide bonds are reduced, releasing NPR1 monomers into the nucleus, where NPR1 acts as a cofactor for transcription factors to induce defense related genes.

Reference

1. George N Agrios, 2005. Plant Pathology 5th Edition pp221- 237

2. Andrea a . gust & thorsten nürnberger . The identification of two receptors for salicylic acid reveals how the hormone controls cell death and survival during plant immune responses, in tissues close to and distant from the site of infection. Plant immunology pp228.

3. Zheng Qing Fu,2012. NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants. Nature doi:10.1038/nature11162

4. Elena T,2006. Hypersensitive cell death in plants – its mechnisms and role in plant defence against pathogens Journal of Fruit and Ornamental Plant Research Vol. 13, 135 -158.