agridif.com The hypersensitive response (HR) triggers localized cell death at the infection site, effectively limiting pathogen spread through rapid and targeted defense mechanisms. Systemic acquired resistance (SAR) provides long-lasting, broad-spectrum immunity by activating defense genes throughout the plant following an initial pathogen attack. Together, HR offers immediate protection, while SAR enhances overall plant resilience against future infections.
Table of Comparison
| Feature | Hypersensitive Response (HR) | Systemic Acquired Resistance (SAR) |
|---|---|---|
| Definition | Localized cell death at infection site to limit pathogen spread | Whole-plant resistance activated after initial infection |
| Activation | Triggered immediately upon pathogen recognition | Activated hours to days after initial infection |
| Scope | Local, confined to infection site | Systemic, affects entire plant |
| Primary Mechanism | Programmed cell death (PCD) to contain pathogens | Induction of pathogenesis-related (PR) proteins |
| Signaling Molecules | Reactive oxygen species (ROS), salicylic acid (local) | Salicylic acid (systemic), methyl salicylate |
| Time Frame | Minutes to hours | Days to weeks |
| Effectiveness | Immediate pathogen containment | Enhanced broad-spectrum disease resistance |
| Key Proteins | Resistance (R) proteins, NADPH oxidases | Pathogenesis-related (PR) proteins like PR-1, PR-5 |
Introduction to Plant Defense Mechanisms
The hypersensitive response (HR) is a localized plant defense that triggers rapid cell death at infection sites to restrict pathogen spread, primarily involving reactive oxygen species and salicylic acid signaling. Systemic acquired resistance (SAR) establishes long-lasting, broad-spectrum immunity throughout the plant by activating pathogenesis-related genes after initial infection. Both HR and SAR are crucial components of plant immune systems, enhancing resistance against diverse pathogens in agricultural contexts.
Overview of Hypersensitive Response (HR)
Hypersensitive response (HR) is a localized plant defense mechanism characterized by rapid cell death at the infection site to restrict pathogen spread. This process involves the accumulation of reactive oxygen species (ROS), production of antimicrobial compounds, and reinforcement of cell walls. HR activates downstream signaling pathways that trigger systemic acquired resistance (SAR), providing long-lasting immunity to distal plant tissues.
Overview of Systemic Acquired Resistance (SAR)
Systemic Acquired Resistance (SAR) is a plant defense mechanism activated after localized exposure to a pathogen, leading to a heightened defense state throughout the entire plant. This process involves the accumulation of salicylic acid and the expression of pathogenesis-related (PR) proteins, which enhance the plant's resistance to a broad spectrum of pathogens. SAR provides long-lasting protection by priming the plant immune system for faster and stronger responses upon subsequent infections.
Molecular Basis of the Hypersensitive Response
The hypersensitive response (HR) in plant pathology involves localized cell death at the infection site, triggered by rapid accumulation of reactive oxygen species (ROS) and salicylic acid (SA) signaling pathways. Key molecular components include resistance (R) proteins that recognize pathogen effector molecules, activating a cascade involving mitogen-activated protein kinases (MAPKs) and transcription factors to upregulate defense genes. This targeted programmed cell death halts pathogen spread, contrasting systemic acquired resistance (SAR), which induces long-lasting, broad-spectrum defense through systemic signaling and pathogenesis-related (PR) proteins.
Molecular Pathways of Systemic Acquired Resistance
Systemic acquired resistance (SAR) is activated through salicylic acid signaling, leading to the accumulation of pathogenesis-related (PR) proteins that enhance plant immunity against a broad spectrum of pathogens. Key molecular components include the NPR1 protein, which regulates the transcription of defense genes by interacting with TGA transcription factors in the nucleus. SAR also involves the mobilization of signaling molecules such as methyl salicylate and azelaic acid, facilitating the systemic spread of defense signals throughout the plant.
Key Signaling Molecules in HR and SAR
Hypersensitive response (HR) in plant defense is primarily mediated by signaling molecules such as reactive oxygen species (ROS), nitric oxide (NO), and salicylic acid (SA), which trigger localized cell death to prevent pathogen spread. Systemic acquired resistance (SAR) relies heavily on salicylic acid accumulation and the systemic signaling molecule methyl salicylate, leading to the activation of pathogenesis-related (PR) genes throughout the plant. Both HR and SAR integrate a complex network of signaling molecules like jasmonic acid and ethylene to fine-tune the immune response against diverse pathogens.
Temporal and Spatial Dynamics of Plant Defense
Hypersensitive response (HR) rapidly initiates localized cell death at the infection site within minutes to hours, effectively restricting pathogen spread through spatial confinement. Systemic acquired resistance (SAR) develops over days, establishing a broad, long-lasting defense throughout distal tissues, enhancing resistance against subsequent infections. The temporal distinction between immediate HR and delayed SAR coordinates spatial defense strategies, balancing localized containment with systemic immunity in plants.
Comparative Effectiveness Against Pathogens
The hypersensitive response (HR) offers rapid localized cell death at infection sites, effectively limiting biotrophic pathogen spread but is less effective against necrotrophs. Systemic acquired resistance (SAR) induces broad-spectrum resistance throughout the plant by activating defense genes, providing long-lasting protection against a wider range of pathogens, including viruses and fungi. Comparative effectiveness highlights HR's immediacy in containment, while SAR ensures durable immunity by priming the entire plant for enhanced defense responses.
Cross-Talk Between HR and SAR Pathways
Hypersensitive response (HR) triggers localized cell death at infection sites, rapidly limiting pathogen spread, while systemic acquired resistance (SAR) induces a broad-spectrum, long-lasting defensive state throughout the plant. Cross-talk between HR and SAR involves signaling molecules such as salicylic acid, reactive oxygen species, and nitric oxide, which coordinate localized and systemic immune responses. This cross-communication optimizes plant defense by integrating immediate pathogen containment with systemic immunity enhancement.
Applications in Crop Disease Management
Hypersensitive response (HR) triggers rapid localized cell death at infection sites, effectively limiting pathogen spread in crops such as potatoes and tomatoes, making it crucial for managing bacterial and viral diseases. Systemic acquired resistance (SAR) provides long-lasting, broad-spectrum protection by activating defense genes throughout the plant, enhancing resilience against future infections like fungal blights in cereals. Integrating HR and SAR strategies, including chemical inducers and resistant cultivars, optimizes crop disease management by reducing reliance on pesticides and improving sustainable agricultural practices.
Related Important Terms
Effector-triggered immunity (ETI)
Effector-triggered immunity (ETI) initiates the hypersensitive response (HR), a localized cell death that restricts pathogen spread at infection sites. Systemic acquired resistance (SAR) follows ETI, activating defense mechanisms throughout the plant to provide long-lasting protection against diverse pathogens.
Pattern-triggered immunity (PTI)
Hypersensitive response (HR) involves localized cell death at the infection site to limit pathogen spread, serving as an early, robust manifestation of pattern-triggered immunity (PTI) by recognizing pathogen-associated molecular patterns (PAMPs). Systemic acquired resistance (SAR) follows HR, activating broad-spectrum defense mechanisms throughout the plant to enhance long-term immunity beyond initial infection zones.
Localized cell death (LCD)
Hypersensitive response (HR) triggers localized cell death (LCD) at infection sites to restrict pathogen spread by confining pathogens within dead cells. Systemic acquired resistance (SAR) activates defense mechanisms throughout the plant without inducing LCD, providing long-lasting protection beyond the initially infected tissue.
Salicylic acid signaling pathway
Hypersensitive response (HR) triggers localized cell death at infection sites through rapid salicylic acid (SA) accumulation, limiting pathogen spread by activating pathogenesis-related (PR) genes. Systemic acquired resistance (SAR) involves long-distance SA signaling that induces broad-spectrum immunity in distal tissues, enhancing durable defense against future pathogen attacks.
Reactive oxygen species burst (ROS burst)
The hypersensitive response (HR) triggers a rapid and localized burst of reactive oxygen species (ROS) at the infection site, leading to programmed cell death that restricts pathogen spread. In contrast, systemic acquired resistance (SAR) involves a sustained and systemic ROS signaling to enhance defense gene expression throughout the plant, providing long-term resistance against secondary infections.
Pathogenesis-related proteins (PR proteins)
The hypersensitive response (HR) involves localized cell death at the infection site, rapidly producing pathogenesis-related (PR) proteins such as chitinases and glucanases to restrict pathogen spread. Systemic acquired resistance (SAR) activates a widespread defense mechanism throughout the plant, elevating the expression of PR proteins including PR-1, PR-2, and PR-5, enhancing long-lasting immunity against diverse pathogens.
Mobile defense signals
The hypersensitive response (HR) triggers localized cell death at infection sites releasing mobile defense signals such as salicylic acid and reactive oxygen species that activate systemic acquired resistance (SAR) throughout the plant. SAR enhances broad-spectrum immunity by promoting expression of pathogenesis-related proteins and reinforcing cell walls in distal tissues to prevent pathogen spread.
Priming of plant immunity
Hypersensitive response (HR) triggers localized cell death at infection sites, creating a rapid barrier to pathogen spread, while systemic acquired resistance (SAR) establishes long-lasting, broad-spectrum immunity throughout the plant by priming defense gene expression. Priming enhances plant immunity by sensitizing defense pathways, enabling faster and stronger activation of responses upon subsequent pathogen attacks.
Epigenetic reprogramming in defense
Hypersensitive response triggers localized cell death to limit pathogen spread, involving rapid epigenetic reprogramming such as DNA methylation and histone modifications that activate defense genes. Systemic acquired resistance enhances long-lasting, broad-spectrum immunity across the plant by epigenetically priming distal tissues, enabling faster and stronger defense gene expression upon subsequent pathogen attack.
SAR-inducing chemical elicitors
Systemic acquired resistance (SAR) in plants is triggered by chemical elicitors such as salicylic acid, benzothiadiazole (BTH), and pipecolic acid, which activate defense genes throughout the plant to enhance resistance against a broad spectrum of pathogens. Unlike the localized hypersensitive response (HR) that causes rapid cell death at infection sites, SAR establishes long-lasting, systemic immunity by priming distal tissues for enhanced defense.
Hypersensitive response vs Systemic acquired resistance for plant defense Infographic
