agridif.com The hypersensitive response (HR) in plant pathology involves rapid, localized cell death at the infection site to restrict pathogen spread, activating defense mechanisms like reactive oxygen species and pathogenesis-related proteins. In contrast, the susceptible response occurs when the plant fails to recognize or effectively respond to the pathogen, leading to disease progression and widespread tissue damage. Understanding these contrasting defense reactions is critical for developing resistant crop varieties and improving disease management strategies.
Table of Comparison
| Aspect | Hypersensitive Response (HR) | Susceptible Response (SR) |
|---|---|---|
| Definition | Rapid localized cell death to restrict pathogen spread | Failure to prevent pathogen invasion, leading to disease |
| Defense Mechanism | Activation of programmed cell death and production of reactive oxygen species (ROS) | Weak or absent immune signaling, pathogen colonization proceeds |
| Pathogen Target | Biotrophic pathogens primarily | Both biotrophic and necrotrophic pathogens |
| Plant Immune Response | Strong effector-triggered immunity (ETI) | Compromised or no effective ETI |
| Outcome | Containment of pathogen, enhanced resistance | Pathogen infection, tissue damage, disease symptoms |
| Examples | Resistance to Pseudomonas syringae in tobacco | Susceptibility to late blight in potato |
Introduction to Plant Defense Mechanisms
Hypersensitive response (HR) in plants triggers rapid localized cell death at infection sites to restrict pathogen spread, activating robust immune signaling pathways such as oxidative bursts and pathogenesis-related protein production. In contrast, susceptible response occurs when the plant fails to recognize or effectively respond to the pathogen, allowing unchecked infection and disease progression. Understanding the molecular basis of HR versus susceptibility is critical for developing disease-resistant crop varieties through genetic engineering or breeding strategies.
Overview of Hypersensitive Response (HR)
The Hypersensitive Response (HR) in plant pathology is a localized, rapid cell death occurring at infection sites, effectively halting pathogen spread by depriving it of nutrients. This programmed cell death is a key component of innate immunity, often triggered by recognition of specific pathogen avirulence (Avr) genes by corresponding plant resistance (R) genes. HR contrasts with susceptible responses where the pathogen successfully colonizes plant tissue, leading to disease development and systemic infection.
Susceptible Response: Definition and Characteristics
Susceptible response in plant pathology refers to the failure of a plant to effectively defend against pathogenic attack, leading to disease development and tissue damage. This response is characterized by pathogen colonization, lack of rapid cell death at the infection site, and the suppression or evasion of plant immune mechanisms. Key indicators include extensive lesion formation, chlorosis, and compromised physiological functions, which ultimately reduce crop yield and plant health.
Molecular Pathways Involved in HR
The hypersensitive response (HR) in plant defense involves a rapid, localized cell death at infection sites, primarily mediated by resistance (R) gene products recognizing pathogen effectors, triggering complex signaling cascades. Key molecular pathways include the activation of mitogen-activated protein kinases (MAPKs), the accumulation of reactive oxygen species (ROS), and the induction of salicylic acid (SA)-dependent signaling that promotes pathogenesis-related (PR) gene expression. In contrast, susceptible responses lack effective R gene recognition and subsequent activation of these defense pathways, allowing pathogen colonization and disease progression.
Pathogen Recognition in HR vs. Susceptible Response
Hypersensitive response (HR) involves rapid and localized cell death at the infection site triggered by specific recognition of pathogen effectors through plant resistance (R) proteins, effectively limiting pathogen spread. In contrast, susceptible response occurs when the plant fails to recognize pathogen effectors, allowing unrestricted pathogen colonization and disease development. HR's pathogen recognition relies on effector-triggered immunity (ETI), whereas susceptible plants mainly depend on inefficient pattern-triggered immunity (PTI) or lack effective R gene-mediated detection.
Cellular Changes During Hypersensitive Response
During the hypersensitive response in plant pathology, cellular changes include rapid cell wall reinforcement, production of reactive oxygen species, and localized programmed cell death to contain pathogen spread. This contrasts with the susceptible response, where these defense mechanisms are weak or absent, allowing pathogen proliferation. Key molecular events involve accumulation of salicylic acid and activation of pathogenesis-related proteins.
Outcomes of Susceptible Response in Plants
The susceptible response in plants results in uncontrolled pathogen growth and widespread tissue damage, often leading to disease symptoms such as wilting, necrosis, and reduced yield. This reaction fails to activate effective defense mechanisms like localized cell death or production of antimicrobial compounds, allowing the pathogen to colonize and exploit the host. Plant susceptibility compromises overall plant health, diminishing resistance and increasing vulnerability to secondary infections.
Genetic Basis of Hypersensitive and Susceptible Responses
The genetic basis of the hypersensitive response (HR) involves specific resistance (R) genes that recognize pathogen avirulence (Avr) genes, triggering localized cell death to prevent pathogen spread. In contrast, the susceptible response occurs when plants lack functional R genes or when pathogens evade recognition, allowing unrestricted disease development. Molecular signaling pathways including salicylic acid and reactive oxygen species are activated in HR, while susceptibility often results from the suppression or evasion of these defense mechanisms at the genetic level.
Role of HR in Disease Resistance Breeding
The hypersensitive response (HR) produces localized cell death at infection sites, effectively limiting pathogen spread and enhancing disease resistance in plants. Breeding programs exploit HR-associated genes to develop cultivars with durable resistance against biotrophic pathogens. Unlike susceptible responses, which allow pathogen colonization, HR triggers rapid immune signaling, activating defense pathways crucial for resistance breeding success.
Comparative Analysis of HR and Susceptible Response
The hypersensitive response (HR) in plants is characterized by rapid localized cell death at the infection site, effectively limiting pathogen spread through programmed cell death and reactive oxygen species accumulation. In contrast, the susceptible response lacks this targeted cell death, allowing pathogens to proliferate and cause disease symptoms due to ineffective activation of defense pathways. Comparative analysis reveals that HR triggers robust immune signaling involving resistance (R) genes and salicylic acid pathways, whereas susceptible responses result from pathogen effector-mediated suppression of host defenses and compromised pathogen recognition.
Related Important Terms
Effector-Triggered Immunity (ETI)
Effector-Triggered Immunity (ETI) activates a hypersensitive response characterized by localized cell death to restrict pathogen spread, contrasting with the susceptible response where the pathogen overcomes the plant's defenses leading to disease progression. The hypersensitive response involves rapid recognition of specific pathogen effectors by plant resistance (R) proteins, triggering robust defense signaling pathways that enhance resistance, whereas in susceptible plants, lack of effective R protein recognition results in failed ETI and increased vulnerability.
Pattern-Triggered Immunity (PTI)
Hypersensitive response (HR) in plant pathology involves rapid, localized cell death at infection sites, effectively limiting pathogen spread by activating Pattern-Triggered Immunity (PTI) through recognition of conserved microbial patterns. In contrast, susceptible response lacks effective PTI activation, allowing pathogen colonization and disease progression due to failure in recognizing or responding to pathogen-associated molecular patterns (PAMPs).
Avr (Avirulence) Gene Recognition
The hypersensitive response in plant pathology is triggered by the recognition of Avr (avirulence) genes by specific R (resistance) genes, leading to localized cell death that restricts pathogen spread. In contrast, the susceptible response occurs when Avr genes are not recognized, allowing the pathogen to proliferate and cause disease.
Lesion Mimic Mutants
Lesion mimic mutants (LMMs) exhibit spontaneous hypersensitive response (HR)-like lesions without pathogen presence, providing crucial insight into programmed cell death and defense signaling pathways in plants. In contrast, susceptible responses lack effective HR activation, allowing pathogen colonization and disease progression, highlighting the essential role of HR in limiting pathogen spread.
Reactive Oxygen Species (ROS) Burst
The hypersensitive response (HR) in plant pathology triggers a rapid and localized Reactive Oxygen Species (ROS) burst, leading to programmed cell death that restricts pathogen spread, while a susceptible response exhibits a delayed or diminished ROS production, allowing pathogen colonization and disease progression. Elevated ROS levels during HR enhance defense signaling pathways and reinforce cell walls through oxidative cross-linking, contrasting with the insufficient oxidative burst observed in susceptible plants.
Programmed Cell Death (PCD)
Hypersensitive response (HR) in plant pathology triggers localized programmed cell death (PCD) to restrict pathogen spread, effectively containing biotrophic infections. In contrast, a susceptible response fails to activate PCD, allowing pathogens to proliferate and cause extensive tissue damage.
Systemic Acquired Resistance (SAR)
Hypersensitive response (HR) triggers localized cell death at infection sites, effectively containing pathogens and activating systemic acquired resistance (SAR) for broad-spectrum defense. In contrast, a susceptible response fails to initiate HR, allowing pathogen proliferation and preventing the establishment of SAR-mediated immunity.
Necrotrophic Effector Sensitivity
The hypersensitive response (HR) in plant pathology triggers localized cell death to restrict biotrophic pathogens, but necrotrophic effectors exploit this by inducing susceptible responses that promote host tissue necrosis and disease progression. Sensitivity to necrotrophic effectors results in enhanced susceptibility, as these toxins manipulate host defense pathways to facilitate necrotrophic pathogen colonization and infection.
Guard Model versus Decoy Model
The Hypersensitive response involves recognition of pathogen effectors by resistance (R) proteins, as explained by the Guard Model where R proteins monitor host targets for effector-induced modifications, triggering localized cell death to restrict infection. In contrast, the Decoy Model describes specialized host proteins that mimic genuine targets, diverting pathogen effectors to activate defense mechanisms without compromising essential cellular functions, highlighting different strategies of immune recognition in plant defense.
Hypersensitive-Induced Resistance (HIR)
Hypersensitive-Induced Resistance (HIR) triggers localized cell death at the infection site, restricting pathogen spread and activating systemic acquired resistance through complex signaling pathways involving salicylic acid and reactive oxygen species. In contrast, a susceptible response fails to contain the pathogen, allowing unchecked colonization and disease progression due to ineffective or suppressed defense mechanisms.
Hypersensitive response vs Susceptible response for defense reaction Infographic
