How Does the Hypersensitive Response Kill Infected Plant Cells?

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How does the hypersensitive response kill infected plant cells? The short answer is that the plant triggers a programmed, localized cell death in the cells a pathogen has reached. The hypersensitive response (HR) is a localized cell death mechanism initiated by the detection of effectors by plant resistance (R) proteins. The dying cells form necrotic lesions, which the sources describe as defense-mediated. This article explains the detection step, the cell death step, and the points the sources do not settle.

Quick answer

• The hypersensitive response is a localized cell death mechanism started when plant resistance proteins detect pathogen effectors.
• Effector-triggered immunity (ETI) produces an oxidative burst that leads to programmed cell death.
• The process produces phytoalexins, which block pathogen spread in the infected tissue.
• The sources describe the outcome well, but they do not give a full step-by-step account of how the dying cell is killed.

How plants detect the invader

Plants use two layers of defense. Pattern recognition receptors in plant cells identify pathogen-associated molecular patterns (PAMPs) and initiate the primary layer of plant immune response, known as pattern-triggered immunity (PTI). The source says that PTI elicits responses including calcium influx and a burst of reactive oxygen species.

The second layer depends on a different class of proteins. The sources state that NLRs solely identify intracellular pathogen effector proteins and initiate immune responses with high specificity. Effectors are proteins that a pathogen delivers inside the plant cell. The NLR proteins are plant resistance proteins, as the viral review’s description of the family makes clear.

The review on plant viruses adds detail about the same family. It describes NB-LRR proteins, which are also called NLRs, and states that these proteins trigger a race-specific reaction reported to be quicker, more robust, and exceeding the threshold of programmed cell death (PCD). That reaction is referred to as the hypersensitive response (HR).

What happens to the infected cell

The fungal review describes the sequence in the plant after detection. The sources state that effector-triggered immunity (ETI) manifests with an oxidative burst that causes defense proteins to increase until it leads to programmed cell death (HR), producing phytoalexins which block pathogen dissemination in the infected tissue.

The same review describes the result as a defense-mediated necrotic lesion. It says that the activation of effector-triggered immunity by viral resistance genes creates defense-mediated necrotic lesions, which are known as hypersensitive responses. A lesion is a patch of dead tissue.

The fungal review also gives a general definition of the mechanism. The hypersensitive response is a localized cell death mechanism initiated by the detection of effectors by plant resistance proteins, providing resistance against biotrophs and hemibiotrophs, and is commonly known as effector-triggered immunity. The word localized is part of the definition.

Why the response is fast and strong

The viral review explains why the response is distinct from a slow infection process. It reports that the reaction is quicker and more robust, and that it exceeds the threshold of programmed cell death. The review describes the hypersensitive response as a race-specific reaction.

The review also describes the NLR protein architecture. It notes that the ARC domain stands for APAF-1, R (plant resistance protein), and CED4, all playing a role in PCD. The sources do not, however, give the full molecular steps that connect the NLR protein to the death of each cell.

Two NLRs can also work together in the cell. The viral review states that many ID-containing NLRs act in a pair with a second NLR, where the ID-NLR is the sensor and the second, a canonical NLR, is the executor acting as a signal transducer. In a sensor and helper arrangement, the sensor detects the effector and passes the signal to a helper NLR. The helpers belong to the RNL class of NLRs, and in the Solanaceae family helper NLRs are of the NRC clade.

How it compares with necrosis caused by pathogens

The fungal review makes a useful distinction. Necrotrophic fungi use effectors to activate host programmed cell death, and their growth depends on dead host tissue. The review states that necrotrophic pathogens pursue growth on the dead host tissues by degrading them before or during colonization period. In that case the pathogen causes the death. In the hypersensitive response, the plant causes the death of its own cells to stop a biotroph or hemibiotroph.

The review also notes that this relationship is not simple. It states that effector-triggered susceptibility (ETS) is characterized by the activation of plant defense mechanisms, frequently resulting in cell death and increased vulnerability to necrotrophic pathogens.

Not all necrosis in infected plants is a defense response. The viral review states that necrosis with no link to resistance has been described for some CMV isolates in many Arabidopsis ecotypes, where it is attributable to protein 1a. Necrosis therefore has more than one cause, and the hypersensitive response is only one of them.

How we chose

The sources were chosen because they are non-retail research reviews on PubMed Central that describe the hypersensitive response directly. One covers the response to plant viruses and the NLR family. The other covers effectors of plant pathogenic fungi and their links to cell death. Both were checked with a direct request that returned HTTP 200 before any quote was used, and every quote in this article comes from the fetched text.

What we could not verify

The sources describe the detection step, the outcome and the defense logic well. They are less complete on the chemistry of the final steps. The points below are the ones the fetched text does not resolve.

What the sources do not say

The sources do not give a single molecular pathway that kills every infected cell. The fungal review describes the oxidative burst, phytoalexins and programmed cell death in general terms, and it does not map each step for one plant and one pathogen. The viral review notes that some questions remain largely unanswered.

The viral review also states that the link between some viral proteins and necrosis remains an open question. It says the question remains largely unanswered, although some observations could suggest such a continuity, since only small changes in a protein can dramatically change the phenotype of infected plants. Readers who need the exact cell death machinery should consult a dedicated plant immunology source.

Frequently asked questions

What is the hypersensitive response in plants?

The hypersensitive response is a localized cell death mechanism initiated when plant resistance proteins detect pathogen effectors. It is also known as effector-triggered immunity.

Why do plant cells die during the hypersensitive response?

The sources describe the cell death as programmed cell death that follows an oxidative burst. The sources link the cell death to the defense response against biotrophs and hemibiotrophs.

What are NLR proteins?

NLRs are plant immune proteins that solely identify intracellular pathogen effector proteins and initiate immune responses with high specificity, according to the sources.

Does the hypersensitive response always protect the plant?

Not always. The fungal review states that effector-triggered susceptibility can result in cell death and increased vulnerability to necrotrophic pathogens.

How is the hypersensitive response different from pattern-triggered immunity?

Pattern-triggered immunity starts with pattern recognition receptors that identify PAMPs and produces responses such as calcium influx and a burst of reactive oxygen species. The hypersensitive response is initiated by NLR proteins that detect effectors and is stronger and more localized.

For related reading, see how the Botrytis fungus kills plant cells and how plants recognize pathogen molecules.

Sources

• The Hypersensitive Response to Plant Viruses, PubMed Central, https://pmc.ncbi.nlm.nih.gov/articles/PMC10612061/
• Effectors of plant pathogenic fungi and fungal like microbes: a comprehensive review on mechanisms, roles, PubMed Central, https://pmc.ncbi.nlm.nih.gov/articles/PMC12339470/