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NF-Y transcription factors are known to play many diverse roles in the development and physiological responses of plants but little is known about their role in plant defense. Here, we demonstrate the negative roles of rice NF-YA family genes in antiviral defense against two different plant viruses, Rice stripe virus (RSV, Tenuivirus ) and Southern rice black-streaked dwarf virus (SRBSDV, Fijivirus ). RSV and SRBSDV both induced the expression of OsNF-YA family genes. Overexpression of OsNF-YAs enhanced rice susceptibility to virus infection, while OsNF-YAs RNAi mutants were more resistant. Transcriptome sequencing showed that the expression of jasmonic acid (JA)-related genes was significantly decreased in plants overexpressing OsNF-YA when they were infected by viruses. qRT-PCR and JA sensitivity assays confirmed that OsNF-YAs play negative roles in regulating the JA pathway. Further experiments showed that OsNF-YAs physically interact with JA signaling transcription factors OsMYC2/3 and interfere with JA signaling by dissociating the OsMYC2/3-OsMED25 complex, which inhibits the transcriptional activation activity of OsMYC2/3. Together, our results reveal that OsNF-YAs broadly inhibit plant antiviral defense by repressing JA signaling pathways, and provide new insight into how OsNF-YAs are directly associated with the JA pathway.

Jasmonic acid (JA) is a crucial hormone in plant antiviral immunity. Increasing evidence shows that viruses counter this host immune response by interfering with JA biosynthesis and signaling. However, the mechanism by which viruses affect JA biosynthesis is still largely unexplored. Here, we show that a highly conserved chloroplast protein cpSRP54 was downregulated in Nicotiana benthamiana infected by turnip mosaic virus (TuMV). Its silencing facilitated TuMV infection. Furthermore, cpSRP54 interacted with allene oxide cyclases (AOCs), key JA biosynthesis enzymes, and was responsible for delivering AOCs onto the thylakoid membrane (TM). Interestingly, TuMV P1 protein interacted with cpSRP54 and mediated its degradation via the 26S proteosome and autophagy pathways. The results suggest that TuMV has evolved a strategy, through the inhibition of cpSRP54 and its delivery of AOCs to the TM, to suppress JA biosynthesis and enhance viral infection. Interaction between cpSRP54 and AOCs was shown to be conserved in Arabidopsis and rice, while cpSRP54 also interacted with, and was degraded by, pepper mild mottle virus (PMMoV) 126 kDa protein and potato virus X (PVX) p25 protein, indicating that suppression of cpSRP54 may be a common mechanism used by viruses to counter the antiviral JA pathway.

The phytohormone gibberellin (GA) is a vital plant signaling molecule that regulates plant growth and defense against abiotic and biotic stresses. To date, the molecular mechanism of the plant responses to viral infection mediated by GA is still undetermined. DELLA is a repressor of GA signaling and is recognized by the F-box protein, a component of the SCF SLY1/GID2 complex. The recognized DELLA is degraded by the ubiquitin-26S proteasome, leading to the activation of GA signaling. Here, we report that ageratum leaf curl Sichuan virus (ALCScV)-infected N . benthamiana plants showed dwarfing symptoms and abnormal flower development. The infection by ALCScV significantly altered the expression of GA pathway-related genes and decreased the content of endogenous GA in N . benthamiana . Furthermore, ALCScV-encoded C4 protein interacts with the DELLA protein NbGAI and interferes with the interaction between NbGAI and NbGID2 to prevent the degradation of NbGAI, leading to inhibition of the GA signaling pathway. Silencing of NbGAI or exogenous GA 3 treatment significantly reduces viral accumulation and disease symptoms in N . benthamiana plants. The same results were obtained from experiments with the C4 protein encoded by tobacco curly shoot virus (TbCSV). Therefore, we propose a novel mechanism by which geminivirus C4 proteins control viral infection and disease symptom development by interfering with the GA signaling pathway.

Potyviridae is the largest family of plant-infecting RNA viruses. All members of the family (potyvirids) have single-stranded positive-sense RNA genomes, with polyprotein processing as the expression strategy. The 5’-proximal regions of all potyvirids, except bymoviruses, encode two types of leader proteases: the serine protease P1 and the cysteine protease HCPro. However, their arrangement and sequence composition vary greatly among genera or even species. The leader proteases play multiple important roles in different potyvirid-host combinations, including RNA silencing suppression and virus transmission. Here, we report that viruses in the genus Arepavirus , which encode two HCPro leader proteases in tandem (HCPro1-HCPro2), can naturally lose the coding sequences for these two proteins during infection. Notably, this loss is associated with a shift in foliage symptoms from severe necrosis to mild chlorosis or even asymptomatic infections. Further analysis revealed that the deleted region is flanked by two short repeated sequences in the parental isolates, suggesting that recombination during virus replication likely drives this genomic deletion. Reverse genetic approaches confirmed that the loss of leader proteases weakens RNA silencing suppression and other critical functions. A field survey of areca palm trees displaying varied symptom severity identified a transitional stage in which full-length viruses and deletion mutants coexist in the same tree. Based on these findings, we propose a scenario in which full-length isolates drive robust infections and facilitate plant-to-plant transmission, eventually giving rise to leader protease-less variants that mitigate excessive damage to host trees, allowing long-term coexistence with the perennial host. To our knowledge, this is the first report of potyvirid self-attenuation via coding sequence loss.

Abstract As research on plant viruses has focused mainly on crop diseases, little is known about these viruses in natural environments. To understand the ecology of viruses in natural systems, comprehensive information on virus–virus and virus–host interactions is required. We applied RNA-Seq to plants from a natural population of Arabidopsis halleri subsp. gemmifera to simultaneously determine the presence/absence of all sequence-reported viruses, identify novel viruses and quantify the host transcriptome. By introducing the criteria of read number and genome coverage, we detected infections by Turnip mosaic virus (TuMV), Cucumber mosaic virus and Brassica yellows virus. Active TuMV replication was observed by ultramicroscopy. De novo assembly further identified a novel partitivirus, Arabidopsis halleri partitivirus 1. Interestingly, virus reads reached a maximum level that was equivalent to that of the host's total mRNA, although asymptomatic infection was common. AhgAGO2, a key gene in host defence systems, was upregulated in TuMV-infected plants. Multiple infection was frequent in TuMV-infected leaves, suggesting that TuMV facilitates multiple infection, probably by suppressing host RNA silencing. Revealing hidden plant–virus interactions in nature can enhance our understanding of biological interactions and may have agricultural applications. RNA-Seq, coupled with de novo assembly, enables the comprehensive and solid determination of virus infection, and revealed the virus–virus and virus–host interactions in naturally growing plants.

Background Southern rice black-streaked dwarf virus (SRBSDV), transmitted by the white-backed planthopper (WBPH), causes severe yield losses in rice across Asia. However, elite resistant germplasms and molecular defense mechanisms remain elusive, hindering breeding efforts. Results Screening of 195 international diverse rice accessions identified a highly resistant (up to 0% disease incidence) variety (R91), exhibiting dual resistance to SRBSDV and rice black-streaked dwarf virus (RBSDV). Multi-omics analysis revealed a rapid defense activation in R91, with an increase in Jasmonic Acid (JA) and Jasmonic Acid-Isoleucine (JA-Ile) by 5 days post-inoculation (dpi), along with upregulation of more than 2,000 defense genes. In contract, susceptible line showed declining JA and JA-Ile level along with suppressed defense responses. Time-ordered co-expression networks pinpointed that OsJAR2 (encoding a JA-Ile synthase, LOC_Os01g12160 ) may act as a hub of resistance molecular network. Genome wide association study (GWAS) identified a novel SRBSDV resistance quantitative trait locus ( qSRBSDV1-1 ) co-localizing with OsJAR2 , and haplotype analysis validated OsJAR2 as the candidate causal resistance gene, further providing genetic evidence for its role in SRBSDV defense. Conclusions Our study identifies a highly SRBSDV-resistant rice germplasm, offering valuable genetic resource for both resistance research and breeding programs. We demonstrate that rapid JA biosynthesis activation and coordinated defense gene expression form the molecular basis of resistance in this accession. Crucially, we pinpoint OsJAR2 as a novel functional resistance gene, with its associated resistant haplotype serving as a robust molecular marker for marker-assisted selection (MAS). These findings advance our understanding of SRBSDV resistance mechanisms and provide a genetic toolkit for developing elite, disease-resistant rice varieties.

Background In the course of long-term confrontation with pathogens, plants have developed complex defense mechanisms to protect themselves from various pathogens. Previous studies have reported that the gibberellin (GA) signaling pathway negative regulator SLENDER RICE 1 (SLR1) in rice activates jasmonic acid (JA)-mediated broad-spectrum antiviral immunity, but the exploration regarding whether OsSLR1 exerts effects on alternative antiviral immune pathways remains limited. Results Here, we identified that OsSLR1 was significantly induced after virus infection and overexpression of OsSLR1 in rice enhance the resistance of rice to southern rice black-streaked dwarf virus (SRBSDV) in rice. Transcriptome analysis revealed that a total of 2,336 differentially expressed genes (DEGs) were detected upon overexpression of OsSLR1 in rice, including 1,607 upregulated genes and 729 downregulated genes. Gene ontology (GO) enrichment analysis and RT-qPCR analysis revealed that genes related to JA and reactive oxygen species (ROS) were significantly upregulated, while genes associated with abscisic acid (ABA) were significantly downregulated. Conclusions These results suggest that OsSLR1 positively regulates the antiviral immunity of rice by modulating multiple pathways.

Background Geminiviruses are circular, single-stranded viruses responsible for enormous crop loss worldwide. Rapid expansion of geminivirus diversity outweighs the continuous effort to control its spread. Geminiviruses channelize the host cell machinery in their favour by manipulating the gene expression, cell signalling, protein turnover, and metabolic reprogramming of plants. As a response to viral infection, plants have evolved to deploy various strategies to subvert the virus invasion and reinstate cellular homeostasis. Main body Numerous reports exploring various aspects of plant-geminivirus interaction portray the subtlety and flexibility of the host–pathogen dynamics. To leverage this pool of knowledge towards raising antiviral resistance in host plants, a comprehensive account of plant’s defence response against geminiviruses is required. This review discusses the current knowledge of plant’s antiviral responses exerted to geminivirus in the light of resistance mechanisms and the innate genetic factors contributing to the defence. We have revisited the defence pathways involving transcriptional and post-transcriptional gene silencing, ubiquitin-proteasomal degradation pathway, protein kinase signalling cascades, autophagy, and hypersensitive responses. In addition, geminivirus-induced phytohormonal fluctuations, the subsequent alterations in primary and secondary metabolites, and their impact on pathogenesis along with the recent advancements of CRISPR-Cas9 technique in generating the geminivirus resistance in plants have been discussed. Conclusions Considering the rapid development in the field of plant-virus interaction, this review provides a timely and comprehensive account of molecular nuances that define the course of geminivirus infection and can be exploited in generating virus-resistant plants to control global agricultural damage.

In 1929, it was reported that yellowing symptoms caused by a tobacco mosaic virus (TMV) yellow mosaic isolate were suppressed in tobacco plants that were systemically infected with a TMV light green isolate. Similar to vaccination, the phenomenon of cross-protection involves a whole plant being infected with an attenuated virus and involves the same or a closely related virus species. Therefore, attenuated viruses function as biological control agents. In Japan, many studies have been performed on cross-protection. For example, the tomato mosaic virus (ToMV)-L11A strain is an attenuated isolate developed by researchers and shows high control efficiency against wild-type ToMV in commercial tomato crops. Recently, an attenuated isolate of zucchini yellow mosaic virus (ZYMV)-2002 was developed and registered as a biological pesticide to control cucumber mosaic disease. In addition, attenuated isolates of pepper mild mottle virus (PMMoV), cucumber mosaic virus (CMV), tobacco mild green mosaic virus (TMGMV), melon yellow spot virus (MYSV), and watermelon mosaic virus (WMV) have been developed in Japan. These attenuated viruses, sometimes called plant vaccines, can be used not only as single vaccines but also as multiple vaccines. In this review, we provide an overview of studies on attenuated plant viruses developed in Japan. We also discuss the application of the attenuated strains, including the production of vaccinated seedlings.

Background Red blotch disease, caused by Grapevine red blotch virus (GRBV, genus Grablovirus , family Geminiviridae ), negatively impacts vine health, fruit yield, and quality, leading to substantial economic losses to growers. While recent studies have enhanced our understanding of the epidemiology of GRBV and its effects, little is known about the molecular basis of the host-virus interactions. Since small RNAs (sRNAs) are known to play a central role in host-virus interactions, this study was undertaken to investigate sRNA dynamics in leaves and berries at two phenological stages (asymptomatic pre- and symptomatic post-véraison) of GRBV-infected grapevines ( Vitis vinifera cv. Merlot). Results Among the 140 microRNAs (miRNAs) detected, 41 isoforms belonging to 18 miRNA families exhibited significant differential expression in response to GRBV infection. Furthermore, 50 miRNAs showed differential expression in samples from pre- and post-véraison stages. A total of 58 conserved and 41 novel targets for known V. vinifera miRNAs were validated using degradome sequencing data from leaf samples of pre- and post-véraison stages. Additionally, virus-derived siRNAs (vsiRNAs) specific to GRBV were present only in GRBV-positive samples. The vsiRNAs predominantly ranged from 19 to 24 nucleotides (nt), with the 21nt size being the most abundant. Mapping vsiRNAs across the GRBV genome revealed an uneven distribution, with vsiRNA-generating hotspots predominantly located in the V3 ORF. Of the 83 most abundant vsiRNAs, grapevine target transcripts were identified for eight of them. Conclusions Identification of differentially expressed miRNAs and vsiRNAs, as well as their targets, offered important insights into various pathways and mechanisms that were affected in grapevine infected with GRBV and in modulating different host responses in leaves and berries. This research serves as a foundation for a better understanding of the molecular interactions in this plant-geminivirus pathosystem.