Hypersensitive Response in Plants

Abstract

The hypersensitive response (HR) is a type of programmed cell death, which is part of the plant's defence response against pathogen attack. In the best of cases, this strategy isolates the pathogens from nutrients during the early steps of infection, causing them to starve before they are able to cause damage. The ability to suppress HR is a major factor for determining whether a pathogen manages to successfully infect a plant. For this reason, HR represents a promising target for improving the overall resistance of crops against pathogens. Attempts to do so are, however, hampered by our lack of understanding how HR is regulated. Signals from the PAMP‐ and effector‐triggered immunity pathways, as well as ROS and phytohormone signals all converge on HR, making it a particularly difficult system to study.

Key Concepts

  • Hypersensitive response is highly complex because of the involvement of many actors.
  • Because of HR, many pathogens starve before they can damage the plant.
  • Signals from PTI, ETI, ROS and phytohormones converge on HR.
  • HR is not an intracellular event, but instead receives input from distant tissues as well.
  • In contrast to early findings, HR is not restricted to the ETI response.
  • How ROS is involved in the HR signalling pathway is still not sufficiently understood.
  • Hypersensitive response often serves as a first line of defence against pathogens, which overcome the preinvasion defences.

Keywords: hypersensitive response; HR; cell death; ROS; pathogen defence

Figure 1. (a): Macroscopic view of a potato leaf, infected with Phytophthora infestans. The dark spots on the leaf's surface are because of the dead cells, which are not the result of the pathogen, but instead the consequence of the hypersensitive response. (b): Microscopic view of HR in a potato leaf.
Figure 2. Inoculation of Arabidopsis (a) or barley (b) with Blumeria graminis f.sp hordei. The tissue was stained with ‘trypan blue’, which colours both fungal and dead plant cells. In cases where the plant is not the host of the pathogen (a), the conidum is either unable to penetrate the plant's cell wall, or immediately triggers HR in the epidermal cells. In host plants (b), the cell wall is penetrated and an haustorium is formed inside the plant cell.
Figure 3. Schematic representation of the progression of HR. Even before the penetrating pathogen reaches the cell membrane, the nucleus migrates towards the pathogen (a–b). The formation of cytoplasmic strands is visible (b), and an increase in nuclear activity is observed (c). After infection, granules start to form (d), and nucleus activity comes to a halt. The nucleus and vacuoles begin to degenerate (e), eventually ending in the collapse of the protoplast (f). Adopted from (Tomiyama, 1956).
Figure 4. Infection of Arabidopsis thaliana with Hyaloperonospora arabidopsidis. The pathogen infects the mesophyll cells, which it penetrates via haustoria. In susceptible plants, the effectors secreted by the pathogen result in a suppression of HR. Resistant plants possess a resistance gene, whereby an ETI response is triggered upon infection, leading to HR. E: Elicitor; R: Resistance protein.
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Camagna, Maurizio, and Takemoto, Daigo(Jan 2018) Hypersensitive Response in Plants. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0020103.pub2]