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The size of viral genomes is limited, thus the majority of encoded proteins possess multiple functions. The main function of tobamoviral movement protein (MP) is to perform plasmodesmata gating and mediate intercellular transport of the viral RNA. MP is a remarkable example of a protein that, in addition to the initially discovered and most obvious function, carries out numerous activities that are important both for the manifestation of its key function and for successful and productive infection in general. Briefly, MP binds the viral genome, delivers it to the plasmodesmata (PD) and mediates its intercellular transfer. To implement the transport function, MP interacts with diverse cellular factors. Each of these cellular proteins has its own function, which could be different under normal conditions and upon viral infection. Here, we summarize the data available at present on the plethora of cellular factors that were identified as tobamoviral MP partners and analyze the role of these interactions in infection development.

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 viruses drive widespread crop epidemics, yet the host plant responses across different cell types, particularly how these responses are influenced by cultivars with varying genetic backgrounds, including the presence of resistance (R) genes, remain poorly understood. Using tomato brown rugose fruit virus (ToBRFV) and two tomato cultivars, ‘Jinpeng No. 1’ (JP) and ‘Rutgers’ (RG), with different genetic backgrounds, this study used single‐cell RNA sequencing to explore infection dynamics and responses at the cellular level. Results showed that ToBRFV accumulated to different levels in the two cultivars, likely due to differences in their genetic backgrounds, particularly the distinct genotypes of the Tm‐22 and tm‐2 alleles. Following infection, the composition of cell types in tomato leaves also varied between the two cultivars. While the entry or movement of ToBRFV in the JP cultivar was not fully prevented early on, the viral accumulation in certain cell types of this cultivar was restricted. ToBRFV alters signalling pathways based on cell type and cultivars. Pseudotime analysis revealed that, in JP plants, ToBRFV reverses expression of brassinosteroid (BR) positive regulators during mesophyll cell development. Silencing positive BR regulators increased infection in JP plants, while suppressing it in RG plants, linking BR signalling to JP‐dependent resistance. Exogenous BR suppressed ToBRFV in JP but enhanced it in RG plants. This study reveals the differential involvement of BR signalling during viral infection in the two cultivars, offering a framework for future studies of plant‐virus interactions.

Summary The tobamovirus tomato brown rugose fruit virus (ToBRFV) has recently emerged, causing significant damage to the tomato industry in various regions worldwide, including the US. ToBRFV evades the widely used Tm‐22 resistance gene, which encodes a nucleotide‐binding leucine‐rich repeat (NLR) class immune receptor with an N‐terminal coiled‐coil (CC) domain that confers resistance to the tomato mosaic virus (ToMV). In this study, we tested a transgenic tomato line (tomatoNN) expressing the Nicotiana glutinosa N gene, which encodes an NLR with a Toll‐Interleukin 1 homology domain (TIR) at the N‐terminus, for resistance to ToBRFV. Our results demonstrate that tomatoNN is resistant to ToBRFV, evidenced by the necrotic local lesions observed on the inoculated leaves and the absence of symptoms on systemic leaves. This correlates with very low to non‐detectable virus levels in double antibody sandwich enzyme‐linked immunosorbent (DAS‐ELISA) and quantitative reverse transcription‐polymerase chain reaction (RT‐qPCR) assays. Furthermore, our findings reveal that tomatoNN is resistant to ToBRFV at 22 °C, but not at 30 °C, showing that the temperature‐sensitive nature of N‐mediated resistance also extends to ToBRFV resistance in tomato. These results highlight the significant potential of using tomatoNN to breed tomato cultivars resistant to ToBRFV, offering a new approach to managing the global pandemic caused by this emerging virus.

Tobamoviruses establish viral replication organelles (VROs) on the host endoplasmic reticulum (ER) for their replication, a process demanding substantial different types of lipids. However, how viruses efficiently transfer these lipids from other compartments like chloroplasts remains incompletely understood. Fibrillin (FBN) proteins are primarily localised to chloroplasts and are intimately linked with lipid metabolism and stress responses in chloroplasts. Here, we report that NbLIP1, a light‐induced FBN1 family protein in Nicotiana benthamiana, directly interacts with the coat protein (CP) of rehmannia mosaic virus (ReMV) and other related tobamoviruses (TMV, YoMV). Upon viral infection, this interaction leads to the relocalisation of NbLIP1 from chloroplasts to ER‐proximal viral replication sites. Functional assays demonstrated that overexpression of NbLIP1 significantly enhanced viral replication, viral protein accumulation, and VRO formation, while silencing NbLIP1 had the opposite effects. These findings unveil a novel viral infection mechanism whereby the viral CP hijacks the host lipid transfer protein NbLIP1 and recruits it to viral replication factories to promote viral replication, potentially by modulating lipid supply or the microenvironment remodelling at the replication sites. This study not only elucidates the role of NbLIP1 as a novel pro‐viral host factor but also provides new insights into how viruses exploit host resources across cellular compartments, suggesting NbLIP1 as a potential antiviral target.

Background Tomato mottle mosaic virus (ToMMV) is a recently identified species in the genus Tobamovirus and was first reported from a greenhouse tomato sample collected in Mexico in 2013. In August 2013, ToMMV was detected on peppers ( Capsicum spp.) in China. However, little is known about the molecular and biological characteristics of ToMMV. Methods Reverse transcription-polymerase chain reaction (RT-PCR) and rapid identification of cDNA ends (RACE) were carried out to obtain the complete genomic sequences of ToMMV. Sap transmission was used to test the host range and pathogenicity of ToMMV. Results The full-length genomes of two ToMMV isolates infecting peppers in Yunnan Province and Tibet Autonomous Region of China were determined and analyzed. The complete genomic sequences of both ToMMV isolates consisted of 6399 nucleotides and contained four open reading frames (ORFs) encoding 126, 183, 30 and 18 kDa proteins from the 5’ to 3’ end, respectively. Overall similarities of the ToMMV genome sequence to those of the other tobamoviruses available in GenBank ranged from 49.6% to 84.3%. Phylogenetic analyses of the sequences of full-genome nucleotide and the amino acids of its four proteins confirmed that ToMMV was most closely related to Tomato mosaic virus (ToMV). According to the genetic structure, host of origin and phylogenetic relationships, the available 32 tobamoviruses could be divided into at least eight subgroups based on the host plant family they infect: Solanaceae-, Brassicaceae-, Cactaceae-, Apocynaceae-, Cucurbitaceae-, Malvaceae-, Leguminosae-, and Passifloraceae-infecting subgroups. The detection of ToMMV on some solanaceous, cucurbitaceous, brassicaceous and leguminous plants in Yunnan Province and other few parts of China revealed ToMMV only occurred on peppers so far. However, the host range test results showed ToMMV could infect most of the tested solanaceous and cruciferous plants, and had a high affinity for the solanaceous plants. Conclusions The complete nucleotide sequences of two Chinese ToMMV isolates from naturally infected peppers were verified. The tobamoviruses were divided into at least eight subgroups, with ToMMV belonging to the subgroup that infected plants in the Solanaceae. In China, ToMMV only occurred on peppers in the fields till now. ToMMV could infect the plants in family Solanaceae and Cucurbitaceae by sap transmission.

Cucumber green mottle mosaic virus (CGMMV), a critical plant virus, has caused significant economic losses in cucurbit crops worldwide. It has not been proved that CGMMV can be transmitted by an insect vector. In this study, the physical contact transmission of CGMMV by Myzus persicae in Nicotiana benthamiana plants was confirmed under laboratory conditions. The acquisition rate increased with time, and most aphids acquired CGMMV at 72 h of the acquisition access period (AAP). Besides, the acquired CGMMV was retained in the aphids for about 12 h, which was efficiently transmitted back to the healthy N . benthamiana plants. More importantly, further experiments suggested that the transmission was mediated by physical contact rather than the specific interaction between insect vector and plant virus. The results obtained in our study contribute to the development of new control strategies for CGMMV in the field.

To establish successful infection, plant viruses produce profound alterations of host physiology, disturbing unrelated endogenous processes and contributing to the development of disease. In tobamoviruses, emerging evidence suggests that viral-encoded proteins display a great variety of functions beyond the canonical roles required for virus structure and replication. Among these, their modulation of host immunity appears to be relevant in infection progression. In this review, some recently described effects on host plant physiology of Tobacco mosaic virus (TMV)-encoded proteins, namely replicase, movement protein (MP) and coat protein (CP), are summarized. The discussion is focused on the effects of each viral component on the modulation of host defense responses, through mechanisms involving hormonal imbalance, innate immunity modulation and antiviral RNA silencing. These effects are described taking into consideration the differential spatial distribution and temporality of viral proteins during the dynamic process of replication and spread of the virus. In discussion of these mechanisms, it is shown that both individual and combined effects of viral-encoded proteins contribute to the development of the pathogenesis process, with the host plant's ability to control infection to some extent potentially advantageous to the invading virus.

Cucumber green mottle mosaic virus (CGMMV) is a Tobamovirus of economic importance affecting cucurbit crops and Asian cucurbit vegetables. Non-host crops of CGMMV, including capsicum (Capsicum annum), sweetcorn (Zea mays), and okra (Abelmoschus esculentus), were tested for their susceptibility to the virus, with field and glasshouse trials undertaken. After 12 weeks post-sowing, the crops were tested for the presence of CGMMV, and in all cases, no CGMMV was detected. Commonly found within the growing regions of cucurbits and melons worldwide are weeds, such as black nightshade (Solanum nigrum), wild gooseberry (Physalis minima), pigweed (Portulaca oleracea), and Amaranth species. Several weeds/grasses were tested for their ability to become infected with CGMMV by inoculating weeds directly with CGMMV and routinely testing over a period of eight weeks. Amaranthus viridis was found to be susceptible, with 50% of the weeds becoming infected with CGMMV. To further analyse this, six Amaranth samples were used as inoculum on four watermelon seedlings per sample and tested after eight weeks. CGMMV was detected in three of six watermelon bulk samples, indicating that A. viridis is a potential host/reservoir for CGMMV. Further research into the relationship between CGMMV and weed hosts is required. This research also highlights the importance of proper weed management to effectively manage CGMMV.

Background Plant breeding research heavily relies on wild species, which harbor valuable traits for modern agriculture. This work employed a new introgression population derived from Solanum pennellii (LA5240), a wild tomato native to Peru, composed of 1,900 genotyped backcross inbred lines (BILs_BC2S6) in the tomato inbreds LEA and TOP cultivated genetic backgrounds. This Peruvian accession was found resistant to the most threatening disease of tomatoes today, caused by the tobamovirus tomato brown rugose fruit virus (ToBRFV). Results The BILs were inoculated and genotyped for 5000 single primer enrichment technology (SPET) markers and phenotyped for virus presence, using ELISA, and for visual symptoms in the terminal shoot, axillary shoots, and fruits. Growth of the recombinant BILs in a highly infected greenhouse enabled the mapping of a quantitative trait locus (QTL) for resistance to ToBRFV to chromosome 2 next to tomato mosaic-1 ( Tm-1 ). The QTL reduced the ELISA values and the symptoms of the axillary shoots in both TOP and LEA BILs. Another locus for resistance was mapped to chromosome 3, which protected the terminal and axillary shoots of the TOP BILs only. A strong QTL for fruit susceptibility to ToBRFV was mapped to chromosome 7 only in the LEA background. Conclusion Taken together, S. pennellii loci conferring resistance and susceptibility act in a tissue-specific manner and are modified by genetic background.