In plants, nucleotide-binding domain and leucine-rich repeat (NLR)-containing proteins can form receptor networks to confer hypersensitive cell death and innate immunity. One class of NLRs, known as NLR required for cell death (NRCs), are central nodes in a complex network that protects against multiple pathogens and comprises up to half of the NLRome of solanaceous plants. Given the prevalence of this NLR network, Derevnina et al. hypothesized that pathogens convergently evolved to secrete effectors that target NRC activities. To test this, they screened a library of 165 bacterial, oomycete, nematode, and aphid effectors for their capacity to suppress the cell death response triggered by the NRC-dependent disease resistance proteins Prf and Rpi-blb2. Among the identified suppressors, the authors found that proteins from a cyst nematode and an oomycete specifically counteract a subset of NRC proteins independently of their sensor NLR partners. The researchers conclude that plant pathogens have evolved to counteract central nodes of the NRC immune receptor network through different mechanisms. The image shows Nicotiana benthamiana leaves infiltrated with Agrobacterium tumefaciens in order to transiently express genes of interest. These brightfield (top left, bottom right) and UV (top right, bottom left) images show N. benthamiana leaves expressing NLR immune receptor mutants that constitutively trigger a form of programmed cell death termed the hypersensitive response. The dead tissue accumulates high amounts of phenolic compounds that fluoresce under UV light, causing the bright green patches observed.

Image Credit: Mauricio P. Contreras