Hypersensitive response: From NLR pathogen recognition to cell death response

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.

Coordinated resource allocation to plant growth–defense tradeoffs

“…Components of the JA-and SA-signaling pathways, with roles in coordination of biotic stress responses, are found in some of the most ancient plant lineages (Wang et al, 2015;Monte et al, 2019;Peñuelas et al, 2019). Some coordination components, such as the TORC-SnRK signaling system, function in similar regulatory roles in all eukaryotes examined to date (van Dam et al, 2011;Roustan et al, 2016;Jamsheer et al, 2019). Thus, while there are some gaps in our knowledge of the ecological context for coordinated resource allocation, we have a strong empirical basis to assume phylogenetic uniformity in the general form of coordination mechanisms.…”

“…ETI signaling includes an acceleration in the hypersensitive response (HR) that produces a fast form of programmed cell death (PCD) at the site of infection (Bruggeman et al, 2015;Radojicic et al, 2018). The ETI responses interact with components of PTI, including the release of ROS and amplification of the HR (Dalio et al, 2021). Necrotic tissue losses during ETI represent an acute cost to G. However, the overall effect is to slow infection during a crucial period of increased secondary metabolite synthesis, which compensates the short-term cost.…”

Geminiviral Triggers and Suppressors of Plant Antiviral Immunity

“…The second level of microbe perception by the host plant is mediated by intracellular immune receptors (R proteins), which recognize pathogen avirulent effectors to activate ETI [3,93,99]. ETI represents a more specific and robust line of host defense, often associated with programmed cell death, HR that restricts the pathogen to the site of infection [100]. Most, but not all, antiviral R proteins harbor a nucleotide-binding leucine-rich repeat (NLR) domain, reminiscent of nonviral intracellular R proteins, which are further classified into coiled-coil (CC)-NLR or Toll/interleukin 1 receptor-like (TIR)-NLR proteins [2,6,101].…”

Oomycete intracellular effectors: specialised weapons targeting strategic plant processes

“…Whereas biotrophs evade or suppress HR, necrotrophs actively cause death in order to feed on lysed tissues. For hemibiotrophs, the moment when PCD occurs can either favour or counteract colonisation (Dalio et al, 2021).…”