Biology subjects

Peng, Y.-L.

Publications and source records attributed to Peng, Y.-L..

5 recordsLinked to original sources

bioRxiv2025

Inactivating a β1 subunit of SnRK1 promotes broad-spectrum disease resistance in rice

Rice is a staple crop for over half of the worlds population, and its sustainable production is vital to ensure global food security. However, rice is highly susceptible to several devastating fungal diseases1, including blast disease caused by Magnaporthe oryzae, sheath blight by Rhizoctonia solani, false smut by Ustilaginoidea virens, brown spot by Bipolaris oryzae, bakanae by Fusarium fujikuroi, and head blight by F. graminearum. The mechanisms underlying the susceptibility of rice to these fungal diseases remain unclear. Here, we report that the {beta} subunit of SnRK1, SnRK1{beta}1A, confers broad-spectrum susceptibility to these fungal diseases. Our findings reveal that diverse rice fungal pathogens have convergently evolved an effector, Gas2, which interacts with SnRK1{beta}1A to prevent its ubiquitination-mediated degradation and promotes its nuclear translocation. While SnRK1{beta}1A is expressed at low levels in healthy plants, its expression is markedly induced upon fungal infections, facilitating susceptibility by inhibiting SnRK11, the subunit of SnRK1, whose overexpression has been shown to enhance broad-spectrum resistance in rice2. Notably, rice lines with disrupted SnRK1{beta}1A are resistant to multiple fungal diseases without compromising growth and yield in the field. Together, this study demonstrates that broad-spectrum disease resistance in crops can be achieved by disrupting inducible susceptibility genes whose encoded proteins are targeted by effectors conserved in multiple pathogens.

plant biology↗

bioRxiv2023

The immune receptor SNC1 monitors helper NLRs targeted by a bacterial effector

Plants deploy intracellular receptors to counteract pathogen effectors that suppress cell-surface receptor-mediated immunity. To what extent pathogens manipulate also immunity mediated by intracellular receptors, and how plants tackle such manipulation, remains unknown. Arabidopsis thaliana encodes three very similar ADR1 class helper NLRs (ADR1, ADR1-L1 and ADR1-L2), which play key roles in plant immunity initiated by intracellular receptors. Here, we report that Pseudomonas syringae AvrPtoB, an effector with E3 ligase activity, can suppress ADR1-L1- and ADR1-L2-mediated cell death. ADR1, however, evades such suppression by diversification of two ubiquitination sites targeted by AvrPtoB. The intracellular sensor NLR SNC1 interacts with and guards the CCR domains of ADR1-L1 and ADR-L2. Removal of ADR1-L1 and ADR1-L2 or delivery of AvrPtoB activates SNC1, which then signals through ADR1 to trigger immunity. Our work not only uncovers the long sought-after physiological function of SNC1 in pathogen defense, but also that reveals how plants can use dual strategies, sequence diversification and a multiple layered guard-guardee system, to counteract pathogen attack on core immunity functions.

plant biology↗

bioRxiv2022

The effector recognition by synthetic sensor NLR receptors requires the concerted action of multiple interfaces within and outside the integrated domain

Plant sensor nucleotide-binding leucine-rich repeat (NLR) receptors detect pathogen effectors through their integrated domains (IDs). The RGA5 sensor NLR recognizes its corresponding effectors AVR-Pia and AVR1-CO39 from the blast fungus Magnaporthe oryzae through direct binding to its heavy metal-associated (HMA) ID to trigger the RGA4 helper NLR-dependent resistance in rice. Here we report a mutant of RGA5 named RGA5HMA5 that confers complete resistance in transgenic rice plants to the M. oryzae strains expressing the noncorresponding effector AVR-PikD. RGA5HMA5 carries three engineered interfaces, two of which lie in the HMA ID and the other in the C-terminal Lys-rich stretch tailing the ID. However, the RGA5 variants having one or two of the three interfaces, including replacing all the Lys residues with Glu residues in the Lys-rich stretch, failed to activate RGA4-dependent cell death of rice protoplasts. Altogether, this work demonstrates that sensor NLRs require a concerted action of multiple surfaces within and outside the IDs to both recognize noncorresponding effectors and activate helper NLR-mediated resistance, and has implications in structure-guided designing of sensor NLRs.

plant biology↗

bioRxiv2020

PacC-dependent adaptation and modulation of host cellular pH controls hemibiotrophic invasive growth and disease development by the rice blast fungus

Many of the worlds most serious crop diseases are caused by hemibiotrophic fungi. These pathogens have evolved the ability to colonize living plant cells, suppressing plant immunity responses, before switching to necrotrophic growth, in which host cells die, providing the energy to fuel sporulation and spread of the fungus. How hemibiotrophic pathogens switch between these two lifestyles remains poorly understood. Here, we report that the devastating rice blast fungus, Magnaporthe oryzae, manipulates host cellular pH to regulate hemibiotrophy. During infection by M. oryzae, host plant cells are alkalinized to pH 7.8 during biotrophic growth, but later acidified to pH 6.5 during necrotrophy. Using a forward genetic screen, we identified alkaline-sensitive mutants of M. oryzae that were blocked in biotrophic proliferation and impaired in induction of host cell acidification and necrotrophy. These mutants defined components of the PacC-dependent ambient pH signal transduction pathway in M. oryzae. We report that PacC exists as a full-length repressor, PacC559, and a truncated transcriptional activator, PacC222, which localize to the fungal nucleus during biotrophic growth and to the cytoplasm during necrotrophy. During biotrophy, PacC222 directly activates genes associated with nutrient acquisition and fungal virulence, while PacC559 represses genes associated with saprophytic mycelial growth and sporulation, which are subsequently de-repressed during necrotrophy. When considered together, our results indicate that temporal regulation of hemibiotrophy by M. oryzae requires PacC-dependent sensing and manipulation of host cellular pH. Author SummaryCrop diseases caused by fungi represent some of the most serious threats to global food security. Many fungal pathogens have evolved the ability to invade living plant tissue and suppress host immunity, before switching to a completely different mode of growth, in which they are able to kill host plant cells. This lifestyle- called hemibiotrophy -is exemplified by the blast fungus, Magnaporthe oryzae, which causes devastating diseases of rice, wheat and many other grasses. We found that during infection by M. oryzae, host cells initially have an alkaline pH, when the fungus is growing in living tissue, but pH rapidly becomes acidic, as host tissue is killed. We identified mutants of the blast fungus that were sensitive to alkaline pH and this enabled us to identify the signal transduction pathway by which the fungus responds to changes in ambient pH. We found that mutants in the pH response pathway were blocked in invasive fungal growth and could not cause acidification of host tissue. Consequently, they are unable to cause blast disease. We characterized the central regulator of this pathway, the PacC transcription factor, which unusually can act as both a repressor and an activator of fungal gene expression. During biotrophic invasive growth, PacC activates many genes previously reported to be required for virulence, including several associated with nutrient acquisition, and at the same time represses genes associated with vegetative growth and sporulation. The PacC signaling pathway is therefore necessary for regulating the switch in fungal lifestyle associated with causing blast disease.

microbiology↗

bioRxiv2020

Comparative secretome of Magnaporthe oryzae identified proteins involved in virulence and cell wall integrity

Plant fungal pathogens secrete numerous proteins into the apoplast at the plant-fungus contact sites to facilitate colonization. Only a few secreted proteins were functionally characterized in Magnaporthe oryzae, the fungal pathogen causing rice blast disease worldwide. ALG3 is an -1, 3-mannosyltransferase function in N-glycan synthesis for secreted N-glycosylated proteins, and the {Delta}alg3 mutants show strong defects in cell wall integrity and fungal virulence, indicating a potential effect on the secretion of multiple proteins. In this study, we compared the secretome of wild type and {Delta}alg3 mutants, and identified 51 proteins that require ALG3 for proper secretion. These are predicted to be involved in metabolic processes, interspecies interactions, cell wall organization, and response to chemicals. The tested secreted proteins localized at the apoplast region surrounding the fungal infection hyphae. Moreover, the N-glycosylation of candidate proteins was significantly changed in the {Delta}alg3 mutant, leading to the reduction of protein secretion and abnormal protein localization. Furthermore, we tested the function of two genes, one is a previously reported M. oryzae gene Invertase 1 (INV1) encoding a secreted invertase, and the other one is a gene encoding an Acid mammalian chinitase (AMCase). The fungal virulence was significantly reduced and the cell wall integrity was altered in the {Delta}inv1 and {Delta}amcase mutant strains. Elucidation of the comparative secretome of M. oryzae improves our understanding of the proteins that require ALG3 for secretion, and of their function in fungal virulence and cell wall integrity.

plant biology↗