Hypersensitive response: From NLR pathogen recognition to cell death response
Citations Over TimeTop 10% of 2020 papers
Abstract
Abstract A wide range of potentially plant pathogenic microorganisms are naturally present in the environment. Despite relying only on the innate immune system, plants are able to resist most of the pathogens. Plants employ a multi‐layered defence system in which the first layer triggers the basal resistance (pathogen‐associated molecular pattern‐triggered immunity [PTI]). The second layer occurs when a resistance protein (R protein) that mostly encodes nucleotide‐binding leucine‐rich repeat receptors (NLRs) recognises an effector molecule secreted by an adapted pathogen, leading to effector‐triggered immunity (ETI), which triggers the hypersensitive response (HR). More recently, ETI was shown to restore and potentiate PTI signalling components, leading to a robust immune response. Multiple mechanisms of regulation are employed to guarantee proper HR activation. NLR proteins can interact between them and form a heel‐like pentamer that anchors to the plasma membrane. Furthermore, NLRs and other proteins can cooperate with NLRs to propagate the immune signalling. Downstream to the recognition of the pathogen by the plant, a rapid cellular response is initiated involving the generation of signalling events that precedes the HR. Here, we summarise the mechanisms involved in HR and highlight new advances in the knowledge of the immune system signalling. We also approach the role of HR threshold during infection by biotrophic, necrotrophic and hemibiotrophic pathogens and the impact in plant fitness and the community of pathogens found in the environment.
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