SummaryPlant sense potential microbial pathogen using pattern recognition receptors (PRRs) to recognize pathogen‐associated molecular patterns (PAMPs). The Lectin receptor‐like kinase genes (LecRKs) are involved in various cellular processes mediated by signal transduction pathways. In the present study, an L‐type lectin receptor kinase gene LecRK‐V was cloned from Haynaldia villosa, a diploid wheat relative which is highly resistant to powdery mildew. The expression of LecRK‐V was rapidly up‐regulated by Bgt inoculation and chitin treatment. Its transcript level was higher in the leaves than in roots, culms, spikes and callus. Single‐cell transient overexpression of LecRK‐V led to decreased haustorium index in wheat variety Yangmai158, which is powdery mildew susceptible. Stable transformation LecRK‐V into Yangmai158 significantly enhanced the powdery mildew resistance at both seedling and adult stages. At seedling stage, the transgenic line was highly resistance to 18 of the tested 23 Bgt isolates, hypersensitive responses (HR) were observed for 22 Bgt isolates, and more ROS at the Bgt infection sites was accumulated. These indicated that LecRK‐V confers broad‐spectrum resistance to powdery mildew, and ROS and SA pathways contribute to the enhanced powdery mildew resistance in wheat.
Stomatal closure defense and apoplastic defense are two major immunity mechanisms restricting the entry and propagation of microbe pathogens in plants. Surprisingly, activation of plant intracellular immune receptor NLR genes, while enhancing whole plant disease resistance, was sometimes linked to a defective stomatal defense in autoimmune mutants. Here we report the use of high temperature and genetic chimera to investigate the inter-dependence of stomatal and apoplastic defenses in autoimmunity. High temperature inhibits both stomatal and apoplastic defenses in the wild type, suppresses constitutive apoplastic defense responses and rescues the deficiency of stomatal closure response in autoimmune mutants. Chimeric plants have been generated to activate NLR only in guard cells or the non-guard cells. NLR activation in guard cells inhibits stomatal closure defense response in a cell autonomous manner likely through repressing ABA responses. At the same time, it leads to increased whole plant resistance accompanied by a slight increase in apoplastic defense. In addition, NLR activation in both guard and non-guard cells affects stomatal aperture and water potential. This study thus reveals that NLR activation has a differential effect on immunity in a cell type specific matter, which adds another layer of immune regulation with spatial information.
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