Natural variations of maize ZmLecRK1 determine its interaction with ZmBAK1 and resistance patterns to multiple pathogens.

Maize (Zea mays) is one of the most important crops in the world, but its yield and quality are seriously affected by diverse diseases. Identifying broad-spectrum resistance genes is crucial for developing effective strategies to control the disease in maize. In a genome-wide study in maize, we identified a G-type lectin receptor kinase ZmLecRK1, as a new resistance protein against Pythium aphanidermatum, one of the causal pathogens of stalk rot in maize. Genetic analysis showed that the specific ZmLecRK1 allele can confer resistance to multiple pathogens in maize. The cell death and disease resistance phenotype mediated by the resistant variant of ZmLecRK1 requires the co-receptor ZmBAK1. A naturally occurring A404S variant in the extracellular domain of ZmLecRK1 determines the ZmLecRK1-ZmBAK1 interaction and the formation of ZmLecRK1-related protein complexes. Interestingly, the ZmLecRK1 susceptible variant was found to possess the amino acid S404 that is present in the ancestral variants of ZmLecRK1 and conserved among the majority of grass species, while the resistance variant of ZmLecRK1 with A404 is only present in a few maize inbred lines. Substitution of S by A at position 404 in ZmLecRK1-like proteins of sorghum and rice greatly enhances their ability to induce cell death. Further transcriptomic analysis reveals that ZmLecRK1 likely regulates gene expression related to the pathways in cell wall organization or biogenesis in response to pathogen infection. Taken together, these results suggest that the ZmLecRK1 resistance variant enhances its binding affinity to the co-receptor ZmBAK1, thereby enhancing the formation of active complexes for defense in maize. Our work highlights the biotechnological potential for generating disease-resistant crops by precisely modulating the activity of ZmLecRK1 and its homologs through targeted base editing.

The Proteomics of Resistance to Halo Blight in Common Bean.

Halo blight disease of beans is caused by a gram-negative bacterium, Pseudomonas syringae pv. phaseolicola. The disease is prevalent in South America and Africa and causes crop loss for indigent people who rely on beans as a primary source of daily nutrition. In susceptible beans, P. syringae pv. phaseolicola causes water-soaking at the site of infection and produces phaseolotoxin, an inhibitor of bean arginine biosynthesis. In resistant beans, P. syringae pv. phaseolicola triggers a hypersensitive response that limits the spread of infection. Here, we used high-throughput mass spectrometry to interrogate the responses to two different P. syringae pv. phaseolicola isolates on a single line of common bean, Phaseolus vulgaris PI G19833, with a reference genome sequence. We obtained quantitative information for 4,135 bean proteins. A subset of 160 proteins with similar accumulation changes during both susceptible and resistant reactions included salicylic acid responders EDS1 and NDR1, ethylene and jasmonic acid biosynthesis enzymes, and proteins enabling vesicle secretion. These proteins revealed the activation of a basal defense involving hormonal responses and the mobilization of extracellular proteins. A subset of 29 proteins specific to hypersensitive immunity included SOBIR1, a G-type lectin receptor-like kinase, and enzymes needed for glucoside and phytoalexin production. Virus-induced gene silencing revealed that the G-type lectin receptor-like kinase suppresses bacterial infection. Together, the results define the proteomics of disease resistance to P. syringae pv. phaseolicola in beans and support a model whereby the induction of hypersensitive immunity reinstates defenses targeted by P. syringae pv. phaseolicola.