A conserved COBL3-like protein promotes PDLP5-dependent callose accumulation to confer broad-spectrum plasmodesmata-mediated antiviral defense.

Suppression of PR1 cleavage-derived peptide-mediated resistance by rhabdovirus glycoprotein facilitates viral transmission by insect vectors in rice.

Pathogenesis-related protein 1 (PR1) serves as a canonical plant defense marker; however, its specific role in conferring resistance against insect herbivores has remained elusive. Here, we delineate a complete PR1-mediated defense pathway in rice. We show that the cysteine protease OsXCP2, in a catalytic residue-dependent manner, cleaves PR1a at the conserved CNYS motif to release the OsCAPE1 peptide, which subsequently activates broad-spectrum resistance against phloem-feeding insects. Insect herbivory induces the co-expression of OsXCP2 and OsPR1a specifically in the phloem. And loss-of-function osxcp2 mutants exhibit compromised resistance, underscoring the functional importance of this pathway in rice anti-herbivore defense. Strikingly, the glycoprotein (G) of the leafhopper-transmitted rhabdovirus rice stripe mosaic virus (RSMV) is secreted into the phloem during viruliferous insect feeding. Mechanistically, RSMV G employs a dual strategy to subvert this defense: it competitively binds the C-terminus of PR1a, thereby blocking OsXCP2-mediated cleavage, and simultaneously sequesters the liberated OsCAPE1 peptide. This concerted inhibition suppresses PR1-dependent resistance against insect feeding and consequently promotes viral transmission. In summary, our study identifies a novel PR1-activated anti-herbivore pathway in rice and reveals a sophisticated viral effector mechanism that antagonizes it to facilitate vector-borne viral transmission.

The hyccin-containing protein ECDR1 interacts with PI3K1 and PI4K1 and regulates broad-spectrum disease resistance in rice.

Programmed cell death and immunity in plants are finely orchestrated to promote antimicrobial defense while preventing autoimmunity. However, the molecular mechanisms involved are not fully understood. Here, we isolated a rice mutant ecdr1 (enhanced cell death and resistance 1) that displayed an autoimmunity phenotype and enhanced resistance to rice blast and bacterial blight, and identified ECDR1 as a new shared component in PI3K and PI4K complexes, linking the hyccin-containing protein with plant defense responses. ECDR1 was expressed at all developmental stages and in all tissues examined. The ECDR1 was highly conserved in function across monocots and dicots. The 113 bp deletion in the ECDR1 promoter reduced its expression, leading to cell death and enhanced disease resistance. The ECDR1 was localized in plasma membrane, and interacted with TPR1 and TPR2 which in turn interacted with both PI4K1 and PI3K1, suggesting that ECDR1 could function as a component associated with not only PI4K complexes but also PI3K complexes to help catalyze PI into PI3P and PI4P. The lethality of all homozygous ecdr1, pi3k1 and tpr1 tpr2 mutants indicated the crucial roles of these genes in plant normal growth, which restricted our understanding of PI3K and PI4K functions. Alternatively, exogenous application of PI3K and PI4K inhibitors could substantially exacerbate the cell death and enhance disease resistance, implying their roles in plant immunity. Our findings provide novel insights into the regulatory mechanisms of ECDR1 in cell death and defense pathways, will aid in understanding the functions of PI3K and PI4K in plant immunity.

The TaLYK5-TaDSK2a module serves as a molecular switch between plant growth and immunity during fungal attack.

It is demonstrated that the TaLYK5-TaDSK2a module functions as a molecular switch that dynamically regulates the trade-off between plant immunity and growth.

A geminivirus satellite-encoded βC1 protein disrupts pipecolic acid-mediated immunity by targeting OSB1 in chloroplasts

Geminiviruses employ sophisticated immune evasion strategies to incite devastating diseases, posing a significant threat to global agricultural security. A central tactic involves the subversion of chloroplast-mediated immunity via viral effectors. Here, we elucidate how the pathogenicity determinant βC1 from ageratum yellow vein China betasatellite (AYVCNB) hijacks this defense system by targeting the chloroplast-localized protein organellar single-stranded DNA-binding protein 1 (OSB1). Functionally, OSB1 acts as a positive regulator of immunity by stabilizing AGD2‐LIKE DEFENSE RESPONSE PROTEIN 1 (ALD1) and promoting pipecolic acid biosynthesis. We demonstrate that AYVCNB-encoded βC1 physically interacts with OSB1, triggering its ubiquitin-proteasome-dependent degradation and consequently abrogating the OSB1-ALD1 defense module. Parallel to this finding, our recent work revealed that βC1 from tomato yellow leaf curl China betasatellite re-localizes OSB1 from the chloroplast to the cytoplasm and promotes its degradation. These results collectively demonstrate that targeting the OSB1-ALD1 defense module represents a widespread and conserved geminivirus mechanism to subvert chloroplast immunity.

MdLYK7 enhances resistance to Valsa canker by activating salicylic acid signaling and PbeBGLU12-mediated fungal cell wall stress.

Down-regulation of VvPLL3 enhances grapevine resistance to Erysiphe necator via defense activation and cell wall remodeling.

Artificial microRNA-based gene silencing approach in PM-susceptible Vitis vinifera cv to stably silence the 'Chardonnay' ortholog of AtPMR6, VvPLL3 improves foliar resistance against the PM fungus.