Shaojie Han

Small open reading frames (sORFs) encoded by plant viruses play critical roles in viral infection. Soybean yellow leaf curl virus (SbYLCV) is a novel monopartite geminivirus causing substantial yield losses in soybean cultivation. In this study, we identified eleven sORFs (designated ORF1-ORF11) in the soybean yellow leaf curl virus (SbYLCV) genome, each predicted to encode peptides ranging from 25 to 100 amino acids. Functional assays revealed that six of these sORFs (ORF2, ORF3, ORF8, ORF9, ORF10, and ORF11) significantly enhanced the pathogenicity of potato virus X. Further analyses demonstrated that the putative proteins encoded by these sORFs exhibit distinct subcellular localization patterns and variable capacities to suppress post-transcriptional gene silencing. Collectively, these results advance our understanding of SbYLCV pathogenesis and offer candidate targets for the development of antiviral strategies against this virus.

Plant-parasitic nematodes are sophisticated metazoan pathogens that deploy complex, animal-like effector repertoires to manipulate host cellular machinery. The Rhg1 locus drives the primary resistance against soybean cyst nematode (Heterodera glycines), yet the mechanism by which its encoded atypical Soluble N-ethylmaleimide-sensitive factor Attachment Protein 18 (SNAP18) proteins restrict this evolutionarily advanced pathogen remains a long-standing enigma. Here, we reveal that Rhg1-mediated resistance operates as a suicide-bait strategy that converts a nematode virulence factor into a selective-autophagic trap. TurboID proximity labeling identified HgGID (glucose-induced degradation), a secreted nematode effector that physically associates with SNAP18 and co-enriches ubiquitin-proteasome components and SNARE-associated factors, consistent with a virulence strategy that engages host trafficking machinery during syncytium formation. Notably, the Rhg1-encoded atypical SNAP18 variant subverts this virulence strategy. We show that HgGID binds all 3 SNAP18 variants, whereas the resistance-associated SNAP18LC/HC variants favor increased dynamic accessibility of the HgGID AIM and promote its ATG8-dependent selective degradation. Ultimately, this targeted autophagic clearance efficiently neutralizes the virulence function of HgGID, establishing a novel paradigm for plant immunity against metazoan pathogens. Our findings uncover a molecular arms race where the host repurposes its vesicle transport machinery into an immune trap, highlighting the central role of selective autophagy in determining the outcome of host-metazoan interactions.

BACKGROUND: Plant‐parasitic nematodes pose severe and growing threats to global agriculture and forestry. However, the development of effective control strategies is limited by the lack of small‐molecule nematicides with well‐defined molecular targets. RESULTS: Three undescribed azaphilones, eutylones A–C ( 1 – 3 ), were isolated from Eutypella sp. NBUF234, a fungus associated with a Cinachyrella sponge collected from the marine mesophotic zone. Their structures were established by spectroscopic analysis, X‐ray crystallography, and quantum chemical calculations. Compounds 2 and 3 represent the first deflectin‐type azaphilones bearing a C‐5 methyl group and a C8 tetraketone side chain. Compounds 1 – 3 showed moderate, dose‐dependent activity against Bursaphelenchus xylophilus (PWN) and Heterodera glycines (SCN). In the 72 h analysis, compound 3 had a lower estimated LC ₅₀ against PWN than compound 2 (90.3 versus 145.8 μM), whereas compounds 2 and 3 had comparable estimated LC ₅₀ values against SCN (159.1 and 159.6 μM). Compound 2 was prioritized for mechanistic profiling based on the preliminary screening results available when those experiments were initiated. Comparative RNA‐seq, proteome‐wide docking, and RNA interference were used to characterize the response to compound 2 . These analyses prioritized CAG9107488.1 as a PWN candidate with preliminary functional support, although direct target engagement was not established. CONCLUSION: Mesophotic sponge‐associated fungi provide structurally novel starting scaffolds for nematicide discovery. The activity ranking was species dependent, and the mechanistic analyses define candidate responses to compound 2 rather than a shared mechanism for all three compounds. Whether compound 3 , which had the lower estimated PWN LC ₅₀ , engages the same response pathway remains to be determined. © 2026 Society of Chemical Industry.

A new Cell study by Wang et al. resolves the long‐elusive biosynthesis and regulation of debneyol, a fungicidal sesquiterpenoid phytoalexin in Solanaceae. The authors define the complete three‐step route from farnesyl pyrophosphate to debneyol and identify the small protein MCD1 as a metabolic organizer that assembles a multienzyme complex to channel flux away from the competing capsidiol branch. The work delivers a roadmap for engineering broad‐spectrum crop resistance and for synthetic biology‐based production of debneyol as a candidate bio‐based crop protectant.

Soybean cyst nematode (SCN, Heterodera glycines ) poses the most devastating biotic threat to global soybean production. Traditional SCN resistance mediated by the Rhg1 locus predominantly relies on gene copy number expansion and elevated α-SNAP protein dosage. Here, we report a novel resistance mechanism in a single-copy rhg1-c background, wherein a C-terminal 24-amino-acid truncation of SNAP18 (designated SNAP18 _lmm3 ) triggers a functional switch from vesicular trafficking to autophagic degradation. Biochemical assays and structural modeling demonstrate that this truncation severely impairs the canonical interaction between SNAP18 and N-ethylmaleimide-sensitive factor (NSF), disrupting SNARE complex recycling and inducing localized cytotoxicity. Concomitantly, the truncated SNAP18 _lmm3 exposes a binding interface for the autophagy-related protein ATG8f, routing the aberrant protein for selective autophagic clearance. This constitutively activated autophagic flux acts as a systemic detoxification system, preventing widespread cell death and ensuring normal plant growth under non-stressed conditions. Upon SCN infection, SNAP18 _lmm3 specifically hyper-accumulates within nematode-induced syncytia. This accumulation reaches levels fourfold higher than in adjacent cells, which overwhelms the local autophagic capacity and triggering targeted cell death that arrests nematode development. By elucidating this competitive molecular switch between NSF and ATG8f binding, our study establishes a “self-degrading toxin” model that resolves the inherent trade-off between plant growth and immunity. This work provides a new theoretical framework for engineering cellular homeostasis to enhance durable crop resistance against parasitic nematodes.

Plant‐parasitic nematodes (PPNs) cause substantial economic losses globally, presenting critical challenges to sustainable agriculture. While chemical nematicides offer short‐term solutions, their environmental and health risks, including adverse effects on nontarget organisms and soil ecosystems, necessitate the development of eco‐friendly alternatives. This review examines chemical and biological approaches to nematode control with a focus on bacterial, fungal, and plant‐derived biocontrol agents, as well as the integration of organic and inorganic soil amendments. These strategies not only manage PPNs but also improve soil structure, fertility, and microbial activity, fostering soil health as the cornerstone of global food security. By synthesizing advancements in nematode management, this review aims to promote sustainable agricultural practices and inspire further research into innovative and effective solutions.