Tomato mosaic virus

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Tomato mosaic virus
Systematics
Classification : Viruses
Area : Riboviria
Empire : Orthornavirae
Phylum : Kitrinoviricota
Class : Alsuviricetes
Order : Martellivirales
Family : Virgaviridae
Genre : Tobamovirus
Type : Tomato mosaic virus
Taxonomic characteristics
Genome : (+) ss RNA
Baltimore : Group 4
Scientific name
Tomato mosaic virus
Short name
ToMV
Left
NCBI  Taxonomy: 12253
ICTV Taxon History: 201855449

The tomato mosaic virus ( scientifically Tomato mosaic virus , acronym ToMV ) is a rigid, rod-shaped plant virus with helical symmetry. It is 300 nm long, 19 nm wide and belongs to the Tobamovirus genus . The genome consists of single-stranded ribonucleic acid approx. 6384 bases in length with positive polarity . As the name suggests, the main host of ToMV is the tomato ( Solanum lycopersicum ). But other plants such as tobacco or paprika can also be usedget infected. The clinical picture manifests itself in leaf necrosis , leaf spotting in the form of mosaics and growth inhibitions .

General

The tomato mosaic virus has been known in the Netherlands and the United States since around 1940. It now occurs wherever tomatoes grow. Because of the high serological agreement with the tobacco mosaic virus (TMV), the tomato mosaic virus was often only regarded as a descendant of the TMV in the 1970s . However, due to the specialization in different host plants, the slightly different protein composition and the different serological affinities, the ToMV is now recognized as an independent virus.

construction

The 300 nm large, linear RNA molecule of the ToMV, with positive polarity, has a length of 6384 nucleotides, which is surrounded by 2128 helically arranged, identical coat proteins. A coat protein consists of 159 amino acids with a molar mass of 17.5 kDa. The extraordinary stability possessed by the virion is based on strong protein-protein interactions (in vitro experiments have shown that the rod structure of the virion is formed even without the presence of RNA) and protein-RNA interactions that the RNA causes when particles form due to restructuring and attachment of further envelope proteins, fix in the resulting tube.

Genome

Like all tobamoviruses also owns the tomato mosaic virus four open reading frames ( english open reading frames , ORFs), three of which encode for non-structural proteins and one for a structural protein. All viral RNAs start at the 5 'end with an m7 cap, followed by a 60-70 nt long untranslated region ( UTR ). Another UTR can also be found at the 3 'end. This is folded into a tRNA -like structure due to incomplete base pairing , which can be aminoacylated with histidine . The ORFs are located between the two UTRs. ORF1 and ORF2 are translated directly from the viral RNA . The product from ORF1 is a 130 kDa protein. In a ratio of 1:10, the product is extended to a fusion protein with the ORF2 due to a “ leaky stop ”. The fusion protein reaches a size of 180 kDa. These translation products together with host proteins form the replicase complex and contain a methyltransferase and a helicase domain . The fusion product also contains the actual polymerase domain . The other two ORFs code for the transport protein (MP) and the coat protein (CP) and are translated by subgenomic mRNAs . First ORF 1 and 2 are read and then ORF 3 and 4. In vivo this process does not take longer than 20 minutes. In vitro replication initiation can be achieved by increasing the pH value to the alkaline range or by the action of detergents such as SDS. The 5 'end is thereby released up to the first start codon . Regulatory functions are ensured by structural areas of the RNA. In the 3 'area within the ORF3, three loops, so-called loops , are formed which contain the origin of assembly (OA), which is absolutely necessary for the initiation of rod formation.

Proteins

The ToMV genome codes for four proteins: The methyltransferase / helicase and the RdR polymerase are responsible for replication. The movement protein (MP) is essential for the spreading from cell to cell within the host and the coat protein (CP, capsid) ensures the protection of the RNA by ensuring the stabilization of the entire virion. In addition, the coat protein plays a role in long-distance transport in the vascular pathways of the plant.

Assembly

The formation of new virus particles takes place in just a few steps. First, a coat protein subunit interacts with the origin of assembly of the RNA. This leads to a change in the conformation of the coat protein and further coat proteins can be attached in the 5 'direction. A helix is ​​formed from which the 5 'end of the RNA is tracked so that the RNA is inside the central channel. Only when the 5 'RNA end is packaged is the 3' end packaged step by step.

illness

The tomato mosaic virus is a plant pathogen; H. it only affects plants and poses no danger to humans, either when it comes into contact with an infected plant or when an infected fruit is consumed. In tomatoes, an infestation can easily be recognized by the mosaic-like staining of the leaves, which differ in the shade of green, and the necroses, especially along the main veins. The virus triggers misshapen growth and narrowing of the leaves, as well as general growth inhibition or dwarfism. The fruits show indentations and necrotic spots, and also a reduction in the yield. The degree of symptoms is strongly dependent on the age, type and nutritional status of the plant as well as on external conditions such as temperature, day length and light intensity. Chlorotic or necrotic local lesions occur in other host plants, and systemic infection in the form of pale green leaves is possible.

Cell to cell spread

The cell walls must be overcome for the virus particles to spread within the plant. The easiest way to do this is to use the already existing connections to the neighboring cells, the plasmodesmata . Substance exchange and signal transmission normally take place via the plasmodesmata. The viruses misuse the plant's transport and communication route for systemic spread. The 30 kDa heavy transport protein ( movement protein , English movement protein , MP) is required for this. The MP is associated with the viral RNA and probably interacts with an as yet unknown receptor on the cytoskeleton in the area of ​​the plasmodesmata. Thereupon an enlargement of the passage opening occurs and the complex of RNA and MP can enter the neighboring cell. Even the widened passage opening is still too narrow for a whole virus particle. If the MP concentration is too high, turgor problems appear in the plant, as the regulating function of the plamodesmata breaks down. The vascular bundles of the plant, mostly the phloem, are used for long-distance transport . Here, too, the virus particles use the information and transport routes of the plant, although other, as yet unknown mechanisms are at work. It has been proven that the coat protein plays a decisive role in this.

Occurrence

ToMV is the most common viral disease in tomatoes. The virus is now endemic to tomatoes around the world. While the tomato is by far the main host of the virus, it is not the only one. ToMV also occurs naturally in peppers, potatoes, cherries, pears and grapes. Symptoms are often chlorotic or necrotic local lesions, but systemic mosaic formation can also occur. In scientific research laboratories, successful infections have also been achieved in many other plant families. A second infection of a tomato plant with the tobacco mosaic virus is a rare event and does not last long. The ToMV stands out from the TMV because of its better adaptation to the host. The TMV replicates and distributes itself much more slowly in the plant, which means that the TMV can also be easily distinguished from the ToMV.

transmission

ToMV infections are aggressive and highly contagious. The ToMV particles are distributed within the crop stands by mechanical cultivation measures. Simple activities are sufficient, such as the use of agricultural equipment or even just the hands, which can cause the smallest wounds in the cuticle or the hairs of the leaves and the virus can first penetrate the plants and, secondly, use tools in the can spread over the entire planted area. In addition, the virus can be absorbed through wounds on the roots through old, virus-containing plant components in the soil or contaminated nutrient solution. The virus remains infectious in the soil for about two years. A third possibility of infection is in the seed itself, because in the case of an infected tomato host plant, the virus also lingers in the seed coat ( testa ) of the seed (but not in the embryo itself) and can thus be spread to other locations by sowing.

prevention

In order to reduce the infection rate in private households and to clean purchased, possibly contaminated seeds and thus to prevent contamination of the soil, thorough washing with warm water is recommended. Thorough hand washing and sterilization of the tools are essential. To be safe from contaminated soil, steaming at a minimum of 90 ° C helps, but this method is quite time-consuming. Once the virus has penetrated the local plant population, only the elimination of infected plants (preferably burned) and the soil around them can help prevent further spread.

Economic impact

The economic damage resulting from infected plants is considerable. The harvest losses can be up to 65%. The desire for a means of control is great in agriculture due to the reduced crop yields, but preventive hygiene and immediate removal of infected plants are the only helpful measures against the spread, unless one resorts to resistant cultivated plants. Once a plant has become infected with the virus, there is no way of getting rid of it without killing the plant. Since there is no natural vector as a carrier (e.g. insects), but this is done by a purely mechanical way, there is also no pesticide or the like with which the spread can be stopped.

For this reason, large breeding programs emerged as early as the 1940s , which worked on breeding resistant lines and establishing them on the market.

Resistances

So far, three naturally occurring, dominant resistance genes for ToMV are known. These are established in cultivated tomatoes and used commercially in this genetically modified form. Tm-1 is from Lycopersicon hirsutum , Tm-2 and Tm-2 2 are both from Lycopersicon peruvianum .

Tm-1

The Tm-1 gene was first discovered from infection experiments with seeds from South America. Infected plants showed no symptoms despite the presence of the virus. In the following decades many breeders tried to introduce the resistant gene into L. esculentum . The backcrossing method was used for this. A homozygous line was generated and the gene was detected on chromosome 5. The mechanism of resistance was deciphered by Motoyoshi and Oshima in 1977, 1979 and by Fraser and co-workers in 1980. It was surprising that the resistance gene interferes with ToMV RNA replication and not, as initially assumed, with the virus uncoating process. It could also be shown that the inhibition of virus replication by the Tm-1 gene is dose-dependent. In addition, they also demonstrated that Tm-1 resistance suppresses symptoms of the disease. These properties made the Tm-1 gene very attractive to plant breeders, but soon after the Tm-1 lines were introduced into commercial breeding, the first ToMV viruses emerged that were able to overcome the resistance. The plants showed the typical mosaic spots. The concentration of viruses found even exceeded the usual amount that is otherwise found in wild-type infected plants. Sequence analyzes showed that all resistance-breaking ToMV strains were exchanges of amino acids in a small region of 150 amino acids (AA) in the C-terminus of the 130kDa methyltransferase / helicase protein. Mutation analyzes showed that there must be at least two amino acid exchanges so that the resistance can be overcome (AS 979 Gln> Glu and AS 984 His> Tyr). These results suggested that the area between aa 900 and 1100 is not important for the function of the proteins during replication, but rather for the interaction with the putative Tm-1 gene product. So the Tm-1 gene product must be an integral part of the replication complex during replication, which was later confirmed by the work of T. Meshi and co-workers.

Tm-2 and Tm-2 2

The second dominant resistance gene for ToMV was isolated for the first time by Soost. The Tm-2 gene reached a higher level of resistance than the Tm-1 gene and was located on chromosome 9. The Tm-2 2 gene is the allele belonging to Tm-2 . Pelham provided the first information regarding the mechanism of resistance to ToMV in 1964. Sometimes necrosis occurred in both genotypes, and indeed in different forms: either it was local necrosis or systemic. The former is referred to by breeders as the hypersensitive reaction (HR) and is a sign of resistance. The systemic reaction occurs as a consequence of incomplete resistance. The development of the necrosis is also temperature and dose dependent. Two naturally occurring ToMV strains, identified by McRitchie and Alexander in Ohio in 1963, were able to overcome the resistance of the Tm-2 genes. All strains that were no longer resistant were classified: ToMV strains that were able to overcome the Tm-1 gene were called ToMV-1, and accordingly all ToMV strains that were able to overcome the Tm-2 gene were called ToMV-2. ToMV strains that could not bypass either of the two resistance genes were classified under ToMV-0. After all ToMV-2 strains had been sequenced, all showed an amino acid exchange in ORF 3, which codes for the movement protein (AA 133 Glu> Lys). The region around the exchange must therefore be important for the recognition of the Tm-2 gene. In contrast to the first two resistance genes, the Tm-2 2 gene remained in use for several years. Here, too, after the sequencing, less surprising due to the allelicity, an amino acid exchange was found in the movement protein, but in several and different places than in the Tm-2 gene (AS 130 Lys> Glu, AS 238 Ser> Arg, AS 244 Lys> Glu). The evolution of the virus strain that can overcome the Tm-2 2 gene thus required more drastic changes in the viral sequence than those of the resistance-breaking viruses of Tm-1 and Tm-2. Molecular analyzes of the alleles Tm-2 and Tm-2 2 were able to show their interaction with the 30kDa-MP of the ToMV with the help of deletion mutants and fusion constructs. The Tm-2 2 gene reacts with the MP in a different, more complex way than does the Tm-2. It requires at least two different binding sites, one at the C-terminus and the second at the N-terminal end of the movement protein.

literature

Individual evidence

  1. ↑ ICTV Master Species List 2018b.v2 . MSL # 34, March 2019
  2. ↑ a b c d ICTV: ICTV Master Species List 2019.v1 , New MSL including all taxa updates since the 2018b release, March 2020 (MSL # 35)
  3. ↑ a b SIB: Tobamovirus , on: ViralZone
  4. ↑ Natural Resistance Mechanism of Plants to Viruses, G. Loebenstein and JP Carr, Springer Verlag