On April 13, 2020, PNAs online published a research paper entitled "patchen manipulation of chloroplast function triggers a light dependent immune recognition" by Professor Wang Yuanchao, School of plant protection, Nanjing Agricultural University.
In animals and plants, leucine repeat (NLR) protein, which is rich in nucleotides, is an intracellular immunosensor, which can recognize and eliminate a variety of invasive pathogens. It is known that NLR mediated immunity is regulated by environmental factors. However, it is not clear how NLRs' recognition of pathogens is influenced by environmental factors such as light. Here, we show that NLR rpi-vnt1.1, which is of agronomic significance, needs light to give the resistant ability of Phytophthora pestis, the pathogen of potato famine in Ireland, to secrete the effector protein avrvnt1. The activation of rpi-vnt1.1 requires nuclear encoded glyk, which is related to energy production. The pathogen effector avrvnt1 binds to the glyk subtype targeted by the full-length chloroplast to activate rpi-vnt1.1. In the dark, rpi-vnt1.1-mediated resistance was impaired because the short glyk (lack of intact chloroplast transport peptide) produced by plants was not bound by avrvnt1. The transition between full-length and shorter plant glyk transcripts is controlled by a light dependent alternative promoter selection mechanism. In plants lacking rpi-vnt1.1, the presence of avrvnt1 can reduce the accumulation of glyk in chloroplasts, thus counteracting the effect of glyk on basic immunity.
Unlike animals, plants lack adaptive immune function and can not actively identify and eliminate invasive pathogens. Therefore, cellular autoimmunity plays an important role in the perception and defense of pathogen infection in plants. Of the cells activated by pattern recognition receptor (PRR) for pathogen related molecular pattern recognition are effective against invaders (innate immune response 1,2). In turn, adaptive pathogens secrete a mixture of effector proteins that inhibit or evade PRR triggered immunity. Some effectors of host translocation are recognized directly or indirectly by highly specialized intracellular immunosensors called nucleotide binding leucine enriched repeat (NLR) (3). The activation of NLRs triggers a strong immune response 4,5 that is usually involved in arresting (known as anaphylaxis (HR) pathogen growth involving local cell death patterns).
In potatoes, the resistance to Phytophthora pestis, the pathogen of potato famine in Ireland, is mainly caused by the coil spiral NLR, which is mostly found in wild Solanaceae species. NLR, named rpi-vnt1.1, which was cloned from Solanaceae, is the first commercial plant disease resistance protein in transgenic crops and has attracted wide attention (6). Rpi-vnt1.1 recognizes a host translocated RXLR type effector protein, called avrvnt1, which is present in all pathogen infected strains currently examined. Although AVR vnt1 showed sequence polymorphism in different isolates, all tested alleles AVR rvnt1 were known to activate rpi-vnt1.1-mediated resistance. The only exception was in pathogenic Phytophthora isolate p13626, from clone EC-1, whose elusive RPI vnt1 recognition was due to downregulation of avrvnt1 gene expression (7). Interestingly, p13527, a closely related strain from the same clone, maintained normal avrvnt1 expression and was recognized by RPI vnt1. Therefore, understanding the underlying mechanism of how rpi-vnt1.1 perceives avrvnt1 can provide information for the rational utilization of this agronomic important resistance gene.