The hypersensitive response (HR) is a defense mechanism that plants employ to protect themselves from invading pathogens. This rapid, localized plant response involves the intentional death of a small number of cells at the site of infection. The primary purpose of this cellular sacrifice is to contain the pathogen, preventing its spread throughout the entire plant body. This is a fundamental part of plant immunity, allowing plants to restrict pathogen growth and ensure their survival.
How Plants Detect Invaders
Plants identify potential threats. Their immune systems recognize specific molecules produced by pathogens, acting as early warning signals. One layer of detection involves recognizing general microbial patterns, called pathogen-associated molecular patterns (PAMPs). These are conserved molecules, such as bacterial flagellin or fungal chitin, common to entire groups of microbes, and are perceived by specialized plant receptors on the cell surface, known as pattern recognition receptors (PRRs).
Beyond these general patterns, plants also recognize specific molecules, called effectors, that pathogens inject into plant cells to manipulate host processes. Plants have an additional layer of defense, effector-triggered immunity (ETI), which relies on specialized resistance (R) proteins. These R proteins detect pathogen effectors. This recognition often occurs when an effector interacts with a host target, triggering a strong defense response.
The Process of Hypersensitive Response
Once a pathogen is recognized, a rapid and localized series of events culminates in the hypersensitive response. This defense involves the swift death of plant cells at the infection site. This programmed cell death (PCD) is a genetically controlled process initiated to isolate the invading pathogen. The dying cells form a barrier, caging the pathogen within a small, necrotic lesion, typically visible as a brown spot on the plant tissue.
Localized cell death deprives biotrophic pathogens, which require living tissue for nutrients, of their food source, halting their spread. This process involves a sudden burst of reactive oxygen species (ROS), such as hydrogen peroxide. This “oxidative burst” contributes to cell death and acts as a signaling molecule. Concurrently, ion fluxes occur across cell membranes, further contributing to cellular collapse. The plant also reinforces cell walls in surrounding healthy cells through callose deposition, creating a physical barrier that restricts pathogen movement.
Plant-Wide Protection
The localized hypersensitive response triggers a broader, systemic defense throughout the entire plant, preparing it for future attacks. This is known as systemic acquired resistance (SAR), providing long-lasting, broad-spectrum protection against a wide range of pathogens. Signals originating from the initial infection site travel through the plant’s vascular system to uninfected leaves and tissues. This long-distance signaling primes distant parts of the plant for an enhanced defense response, meaning they will react more quickly and strongly if a secondary infection occurs.
A primary signaling molecule involved in SAR is salicylic acid (SA), a plant hormone that accumulates in both the infected and uninfected tissues. Salicylic acid activates a signaling cascade that leads to the expression of various defense-related genes, including pathogenesis-related (PR) proteins. These PR proteins can directly inhibit pathogen growth or strengthen plant cell walls, making them more resistant to future penetration. The induced resistance provided by SAR can persist for weeks or even months, offering a durable form of plant immunity.