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Tomato cultivars containing the Tm‐22 resistance gene have been widely known to resist tobacco mosaic virus (TMV) and tomato mosaic virus. Tomato brown rugose fruit virus (ToBRFV), a new emerging tobamovirus, can infect tomato plants carrying the Tm‐22 gene. However, the virulence determinant of ToBRFV that overcomes the resistance conferred by the Tm‐22 gene remains unclear. In this study, we substituted the movement protein (MP) encoding sequences between ToBRFV and TMV infectious clones and conducted infectivity assays. The results showed that MP was the virulence determinant for ToBRFV to infect Tm‐22 transgenic Nicotiana benthamiana plants and Tm‐22‐carrying tomato plants. A TMV MP chimera with amino acid residues 60–186 of ToBRFV MP failed to induce hypersensitive cell death in the leaves of Tm‐22 transgenic N. benthamiana plants. Chimeric TMV containing residues 60–186 of ToBRFV MP could, but chimeric ToBRFV containing 61–187 residues of TMV MP failed to infect Tm‐22 transgenic N. benthamiana plants, indicating that 60–186 residues of MP were important for ToBRFV to overcome Tm‐22 gene‐mediated resistance. Further analysis showed that six amino acid residues, H67, N125, K129, A134, I147, and I168 of ToBRFV MP, were critical in overcoming Tm‐22‐mediated resistance in transgenic N. benthamiana plants and tomato plants. These results increase our understanding of the mechanism by which ToBRFV overcomes Tm‐22‐mediated resistance. Six amino acid residues, H67, N125, K129, A134, I147, and I168, located in the central region of the movement protein are involved in tomato brown rugose fruit virus to evade Tm‐22‐mediated resistance.

Eukaryotic translation initiation factor 4E (eIF4E), which plays a pivotal role in initiating translation in eukaryotic organisms, is often hijacked by the viral genome‐linked protein to facilitate the infection of potyviruses. In this study, we found that the naturally occurring amino acid substitution D71G in eIF4E is widely present in potyvirus‐resistant watermelon accessions and disrupts the interaction between watermelon eIF4E and viral genome‐linked protein of papaya ringspot virus‐watermelon strain, zucchini yellow mosaic virus or watermelon mosaic virus. Multiple sequence alignment and protein modelling showed that the amino acid residue D71 located in the cap‐binding pocket of eIF4E is strictly conserved in many plant species. The mutation D71G in watermelon eIF4E conferred resistance against papaya ringspot virus‐watermelon strain and zucchini yellow mosaic virus, and the equivalent mutation D55G in tobacco eIF4E conferred resistance to potato virus Y. Therefore, our finding provides a potential precise target for breeding plants resistant to multiple potyviruses. The amino acid substitution D71G in the cap‐binding pocket of watermelon eIF4E and its equivalent substitution D55G in tobacco eIF4E confers resistance to multiple potyviruses by disrupting the interaction between eIF4E and VPg.

Stalk rot, primarily caused by Fusarium graminearum ( Fg ) and Pythium inflatum ( Pi ), is a major maize disease responsible for significant yield losses. The molecular mechanisms governing defence against these pathogens remain poorly understood. To uncover key miRNAs and their regulatory genes, small RNA, degradome, and transcriptome sequencing data were integrated to explore maize's response to stalk rot. A total of 363 miRNAs, including 113 novel ones, were identified from 12 sRNA libraries, with 305 differentially expressed miRNAs (DEMs) significantly responding to Fg and Pi infection. Degradome analysis detected 120 DEMs. Through transcriptome sequencing and weighted gene co‐expression network analysis (WGCNA), 6 Fg / Pi ‐responsive regulatory modules, centered on hub genes, were identified from 8308 differentially expressed genes activated or repressed by the two pathogens. A machine‐learning approach revealed complex regulatory networks within these significant pathogen‐responsive modules. WGCNA highlighted ZmMYB74 , targeted by zma–miR319, as a key hub gene regulator in these networks. Transgenic plants overexpressing ZmMYB74 showed compromised resistance to stalk rot pathogens, with reduced lignin deposition, whereas knockout or suppression of ZmMYB74 resulted in significantly enhanced resistance. Two In/Dels in the promoter region associated with ZmMYB74 transcription were linked to changes in maize resistance to stalk rot. ZmMYB74 functions as a transcriptional repressor, negatively regulating the expression of ZmCAD , a positive regulator of plant disease resistance involved in lignin biosynthesis. Isolating the resistance gene ZmMYB74 will not only aid in developing durable disease‐resistant maize varieties but also enhance understanding of the molecular mechanisms underlying stalk rot resistance.

Sugarcane mosaic virus (SCMV; genus Potyvirus ) induces maize dwarf mosaic disease that has caused serious yield losses of maize in China. Cross-protection is one of the efficient strategies to fight against severe virus strains. Although many mild strains have been identified, the spontaneous mutation is one of the challenging problems affecting their application in cross-protection. In this study, we found that the substitution of cysteine (C) at positions 57 or 60 in the zinc finger-like motif of HC-Pro with alanine (A; C57A or C60A) significantly reduced its RNA silencing suppression activity and SCMV virulence. To reduce the risk of mild strains mutating to virulent ones by reverse or complementary mutations, we obtained attenuated SCMV mutants with double-mutations in the zinc finger-like and FRNK motifs of HC-Pro and evaluated their potential application in cross-protection. The results showed that the maize plants infected with FKNK/C60A double-mutant showed symptomless until 95 days post-inoculation and FKNK/C60A cross-protected plants displayed high resistance to severe SCMV strain. This study provides theoretical and material bases for the control of SCMV through cross-protection.

Summary To establish systemic infection, plant viruses must replicate, and conduct intra‐ and intercellular movement and long‐distance movement, all of which require the participation of host factors. Tobamoviruses move in the form of movement protein (MP)–viral RNA complex and utilize endocytosis for intracellular movement. However, how tobamoviral MPs hijack host factors to reach the plasma membrane (PM) and then plasmodesmata (PD) is still largely unknown. Tomato brown rugose fruit virus (ToBRFV) is an emerging tobamovirus that mainly infects tomatoes and peppers. Here, we show that tomato RabE1a, a small Rab GTPase, interacts with ToBRFV MP and participates in the movement of ToBRFV. Knocking out RabE1a in tomatoes could inhibit infection by ToBRFV. RabE1a positively regulates MP transport to the PM, and this transport process is regulated by its nucleotide‐binding state. Furthermore, RabE1a interacts with the exocyst subunit SEC10b to jointly regulate MP transport to the PM and intracellular movement of ToBRFV. The adaptor protein AP2β interacts with MP and transports MP from the PM to the PD for intercellular movement of ToBRFV. We further find that knocking out RabE1a could also inhibit the infection of other tobamoviruses. In summary, MP exocytosis is coregulated by RabE1a and the exocyst subunit SEC10b for transport to the PM, where it then uses AP2β‐regulated endocytosis to PD. These results provide a comprehensive overview of tobamoviral MP intracellular transport and are insightful for breeding tomato plants resistant to ToBRFV and related tobamoviruses.

Plant resistance, which acts as a selective pressure that affects viral population fitness, leads to the emergence of resistance‐breaking virus strains. Most recessive resistance to potyviruses is related to the mutation of eukaryotic translation initiation factor 4E (eIF4E) or its isoforms that break their interactions with the viral genome‐linked protein (VPg). In this study, we found that the VPg α1–α2 loop, which is essential for binding eIF4E, is the most variable domain of papaya ringspot virus (PRSV) VPg. PRSV VPg with the naturally occurring amino acid substitution of K105Q or E108G in the α1–α2 loop fails to interact with watermelon (Citrullus lanatus) eIF4E but interacts with watermelon eIF(iso)4E instead. Moreover, PRSV carrying these mutations can break the eIF4E‐mediated resistance to PRSV in watermelon accession PI 244019. We further revealed that watermelon eIF(iso)4E with the amino acid substitutions of DNQS to GAAA in the cap‐binding pocket could not interact with PRSV VPg with natural amino acid substitution of K105Q or E108G. Therefore, our finding provides a precise target for engineering watermelon germplasm resistant to resistance‐breaking PRSV isolates. Papaya ringspot virus isolates with amino acid substitution of K105Q or E108G in VPg can break the eIF4ED71G‐mediated resistance by re‐hijacking another susceptibility factor eIF(iso)4E in watermelon.

Cross-protection is a promising measure to control plant viral diseases. Reverse genetics had been recently adopted to generate attenuated mutants that have potential in cross-protection. But studies on the variability of the progeny viruses of the attenuated mutants are scarce. Sugarcane mosaic virus (SCMV; genus Potyvirus , family Potyviridae ) is the prevalent virus inducing maize dwarf mosaic disease in China. Here, we showed that the substitution of arginine with isoleucine in the FRNK motif at position 184 of helper component-proteinase (HC-Pro) abolished its RNA silencing suppression (RSS) activity, drastically reduced the virulence and accumulation level of SCMV, and impaired the synergism between SCMV and maize chlorotic mottle virus. The attenuated mutant could protect maize plants from a severe infection of SCMV. However, a spontaneous mutation of glycine at position 440 to arginine in HC-Pro rescued the virulence and synergism with maize chlorotic mottle virus of SCMV and the RSS activity of HC-Pro. Similar results were obtained with tobacco vein banding mosaic virus and watermelon mosaic virus. These results provide novel evidence for the complementary mutation of potyviruses in maintaining the HC-Pro RSS activity and potyviral virulence and remind us of evaluating the potential risk of attenuated mutants thoroughly before applying for the control of plant viral diseases via cross-protection.

Plant virus‐based vectors are gaining significant attention as bioreactors for recombinant protein production due to their broad host range, robust expression levels and cost‐effectiveness; however, their practical utility is frequently constrained by severe viral pathogenicity. Notably, the utility of potato virus Y (PVY), the type member of the genus Potyvirus, is severely hampered by its elicitation of tobacco vein necrosis (TVN). Here, we demonstrate that a single synonymous substitution (AAA to AAG) at the K178 codon of P1 causes almost no TVN. Mechanistically, the P1‐AAG mutation attenuates the synergistic RNA silencing suppression (RSS) activity typically mediated by the P1/HC‐Pro complex. This functional impairment abrogates the virus‐induced upregulation of specific host microRNAs (miR6020, miR6164 and miR6021). Using this non‐necrotic PVY‐P1‐AAG vector, we engineered an optimised bioproduction platform. By integrating a GFP‐HRV3C fusion tag system with affinity purification and subsequent proteolytic cleavage, we achieved the high‐yield synthesis of recombinant human interferons (IFN‐α1b and IFN‐α2b) in Nicotiana benthamiana and Nicotiana tabacum ‘Xanthi’. Codon optimisation of the cargo genes further enhanced protein accumulation, achieving yields of up to 55.2 μg/g fresh leaf weight. Taken together, these results provide new insights into how synonymous substitutions influence potyviral pathogenicity and validate the symptomless P1‐AAG vector as a robust system for biomanufacturing value‐added proteins. A synonymous mutation at P1 K178 attenuates PVY virulence and abolishes tobacco vein necrosis. This attenuated vector serves as a high‐efficiency plant bioreactor for the production and purification of recombinant human interferons.

Preterm birth is a leading global cause of neurodevelopmental impairment (NDI), yet early predictive biomarkers remain elusive. The gut microbiome, developing in parallel with the brain and communicating via the microbiota-gut-brain axis, holds potential as a source of such biomarkers. However, specific longitudinal multi-omics signatures predictive of NDI risk in preterm infants are poorly defined. We conducted a prospective, matched, longitudinal study of 60 preterm infants, classified at 3 months corrected age (CA) into high-risk (HR, n=30) or low-risk (LR, n=30) groups for NDI based on combined motor (TIMP) and neurological (GMs) assessments. Fecal samples from birth (meconium) and 3 months CA underwent shotgun metagenomic sequencing and untargeted metabolomics. Groups were rigorously matched for gestational age, birth weight, sex, and clinical exposures. While α- and β-diversity did not differ between groups, profound taxonomic and functional divergence emerged. At 3 months CA, the LR gut was enriched with Akkermansia muciniphila , whereas the HR gut was dominated by Klebsiella variicola . Functional metagenomics revealed a dysbiotic HR trajectory, enriching pathways for bacterial virulence, stress response, and—notably—multiple pathways annotated for human neurodegenerative diseases, contrasting with LR expansion of core biosynthesis. Metabolomics confirmed a dysfunctional HR state, showing impaired amino acid metabolism and aberrant neuroactive pathway enrichment. Critically, meconium features correlated with 3-month neurobehavioral scores, demonstrating ultra-early predictive potential. Integrated networks at 3 months directly linked Akkermansia muciniphila and co-varying glycerophospholipids to superior neurodevelopmental scores, forming a beneficial “ Akkermansia -lipid” axis, while Klebsiella variicola and triterpenoids formed a dysbiotic hub. Our study defines a high-risk gut ecosystem trajectory in preterm infants, characterized by early commensal depletion, pathobiont expansion, and a functional shift towards inflammation and neuroinflammation. These signatures offer novel targets for early risk prediction and microbiome-targeted interventions.