Publications by authors named "Minhang Yuan"

Plant stomata open in response to blue light, allowing gas exchange and water transpiration. However, open stomata are potential entry points for pathogens. Whether plants can sense pathogens and mount defense responses upon stomatal opening and how blue-light cues are integrated to balance growth-defense trade-offs are poorly characterized.

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Reactive oxygen species (ROS) and phosphatidic acid (PA) are important second messengers in plant immunity. PA binding to RBOHD, an NADPH oxidase responsible for ROS production, enhances RBOHD stability and promotes ROS production. Distinct phosphorylation of the lipid kinase DGK5 optimizes the PA burst in regulating ROS production.

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Biphasic production of reactive oxygen species (ROS) has been observed in plants treated with avirulent bacterial strains. The first transient peak corresponds to pattern-triggered immunity (PTI)-ROS, whereas the second long-lasting peak corresponds to effector-triggered immunity (ETI)-ROS. PTI-ROS are produced in the apoplast by plasma membrane-localized NADPH oxidases, and the recognition of an avirulent effector increases the PTI-ROS regulatory module, leading to ETI-ROS accumulation in the apoplast.

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Phytopathogens like Pseudomonas syringae induce "water soaking" in the apoplastic space of plant leaf tissue as a key virulence mechanism. Water soaking is commonly observed in diverse pathosystems, yet the underlying physiological basis remains largely elusive. Here, we show that one of the strong P.

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pathosystem has been used as an important model system for studying plant-microbe interactions, leading to many milestones and breakthroughs in the understanding of plant immune system and pathogenesis mechanisms. Bacterial infection and plant disease assessment are key experiments in the studies of plant-pathogen interactions. The hypersensitive response (HR), which is characterized by rapid cell death and tissue collapse after inoculation with a high dose of bacteria, is a hallmark response of plant effector-triggered immunity (ETI), one layer of plant immunity triggered by recognition of pathogen-derived effector proteins.

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The plant immune system is fundamental for plant survival in natural ecosystems and for productivity in crop fields. Substantial evidence supports the prevailing notion that plants possess a two-tiered innate immune system, called pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is triggered by microbial patterns via cell surface-localized pattern-recognition receptors (PRRs), whereas ETI is activated by pathogen effector proteins via predominantly intracellularly localized receptors called nucleotide-binding, leucine-rich repeat receptors (NLRs).

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Plants resist attacks by pathogens via innate immune responses, which are initiated by cell surface-localized pattern-recognition receptors (PRRs) and intracellular nucleotide-binding domain leucine-rich repeat containing receptors (NLRs) leading to pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), respectively. Although the two classes of immune receptors involve different activation mechanisms and appear to require different early signalling components, PTI and ETI eventually converge into many similar downstream responses, albeit with distinct amplitudes and dynamics. Increasing evidence suggests the existence of intricate interactions between PRR-mediated and NLR-mediated signalling cascades as well as common signalling components shared by both.

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Population structure and relationship analysis is of great importance in the germplasm utilization and association mapping. Jute, comprised of white jute (C. capsularis L) and dark jute (C.

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