Wu, C.-h. | Search bioRxiv

bioRxiv2021

Rpi-amr3 confers resistance to multiple Phytophthora species by recognizing a conserved RXLR effector

Diverse pathogens from the genus Phytophthora cause disease and reduce yields in many crop plants. Although many Resistance to Phytophthora infestans (Rpi) genes effective against potato late blight have been cloned, few have been cloned against other Phytophthora species. Most Rpi genes encode nucleotide-binding domain, leucine-rich repeat-containing (NLR) proteins, that recognize RXLR effectors. However, whether NLR proteins can recognize RXLR effectors from multiple different Phytophthora pathogens has rarely been investigated. Here, we report the effector AVRamr3 from P. infestans that is recognized by Rpi-amr3 from S. americanum. We show here that AVRamr3 is broadly conserved in many different Phytophthora species, and that recognition of AVRamr3 homologs enables resistance against multiple Phytophthora pathogens, including P. parasitica and P. palmivora. Our findings suggest a novel path to identifying R genes against important plant pathogens.

plant biology↗

bioRxiv2021

Plant pathogens convergently evolved to counteract redundant nodes of an NLR immune receptor network

In plants, NLR (nucleotide-binding domain and leucine-rich repeat-containing) proteins can form receptor networks to confer hypersensitive cell death and innate immunity. One class of NLRs, known as NRCs (NLR required for cell death), 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, we hypothesized that pathogens convergently evolved to secrete effectors that target NRC activities. To test this, we screened a library of 167 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 five of the identified suppressors, one cyst nematode protein and one oomycete protein suppress the activity of autoimmune mutants of NRC2 and NRC3, but not NRC4, indicating that they specifically counteract a subset of NRC proteins independently of their sensor NLR partners. Whereas the cyst nematode effector SPRYSEC15 binds the nucleotide-binding domain of NRC2 and NRC3, the oomycete effector AVRcap1b suppresses the response of these NRCs via the membrane trafficking-associated protein NbTOL9a (Target of Myb 1-like protein 9a). We conclude that plant pathogens have evolved to counteract central nodes of the NRC immune receptor network through different mechanisms. Coevolution with pathogen effectors may have driven NRC diversification into functionally redundant nodes in a massively expanded NLR network.

plant biology↗