TOBACCO MOSAIC VIRUS. (TMV)

Tobacco mosaic virus (TMV) is a positive-sense single-stranded RNA virus species in the genus Tobamovirus that infects a wide range of plants, especially tobacco and other members of the family Solanaceae. The infection causes characteristic patterns, such as "mosaic"-like mottling and discoloration on the leaves (hence the name). TMV was the first virus to be discovered. Although it was known from the late 19th century that a non-bacterial infectious disease was damaging tobacco crops, it was not until 1930 that the infectious agent was determined to be a virus. It is the first pathogen identified as a virus. The virus was crystallised by W.M. Stanley. It has a similar size to the largest synthetic molecule, known as PG5.[1]

Tobacco mosaic virus

Transmission electron micrograph of TMV particles negative stained to enhance visibility at 160,000× magnification

Transmission electron micrograph of TMV particles negative stained to enhance visibility at 160,000× magnification

Virus classificationEdit this classification

(unranked):

Virus

Realm:

Riboviria

Kingdom:

Orthornavirae

Phylum:

Kitrinoviricota

Class:

Alsuviricetes

Order:

Martellivirales

Family:

Virgaviridae

Genus:

Tobamovirus

Species:

Tobacco mosaic virus

History

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In 1886, Adolf Mayer first described the tobacco mosaic disease that could be transferred between plants, similar to bacterial infections.[2][3] In 1892, Dmitri Ivanovsky gave the first concrete evidence for the existence of a non-bacterial infectious agent, showing that infected sap remained infectious even after filtering through the finest Chamberland filters.[3][4] Later, in 1903, Ivanovsky published a paper describing abnormal crystal intracellular inclusions in the host cells of the affected tobacco plants and argued the connection between these inclusions and the infectious agent.[5] However, Ivanovsky remained rather convinced, despite repeated failures to produce evidence, that the causal agent was an unculturable bacterium, too small to be retained on the employed Chamberland filters and to be detected in the light microscope. In 1898, Martinus Beijerinck independently replicated Ivanovsky's filtration experiments and then showed that the infectious agent was able to reproduce and multiply in the host cells of the tobacco plant.[3][6] Beijerinck adopted the term of "virus" to indicate that the causal agent of tobacco mosaic disease was of non-bacterial nature. Tobacco mosaic virus was the first virus to be crystallized. It was achieved by Wendell Meredith Stanley in 1935 who also showed that TMV remains active even after crystallization.[3] For his work, he was awarded 1/4 of the Nobel Prize in Chemistry in 1946,[7][8] even though it was later shown some of his conclusions (in particular, that the crystals were pure protein, and assembled by autocatalysis) were incorrect.[9] The first electron microscopical images of TMV were made in 1939 by Gustav Kausche, Edgar Pfankuch and Helmut Ruska – the brother of Nobel Prize winner Ernst Ruska.[10] In 1955, Heinz Fraenkel-Conrat and Robley Williams showed that purified TMV RNA and its capsid (coat) protein assemble by themselves to functional viruses, indicating that this is the most stable structure (the one with the lowest free energy). The crystallographer Rosalind Franklin worked for Stanley for about a month at Berkeley, and later designed and built a model of TMV for the 1958 World's Fair at Brussels. In 1958, she speculated that the virus was hollow, not solid, and hypothesized that the RNA of TMV is single-stranded.[11] This conjecture was proven to be correct after her death and is now known to be the + strand.[12] The investigations of tobacco mosaic disease and subsequent discovery of its viral nature were instrumental in the establishment of the general concepts of virology.[3]

Structure

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Structure

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Schematic model of TMV: 1. nucleic acid (RNA), 2. capsomer protein (protomer), 3. capsid

Tobacco mosaic virus has a rod-like appearance. Its capsid is made from 2130 molecules of coat protein and one molecule of genomic single strand RNA, 6400 bases long. The coat protein self-assembles into the rod-like helical structure (16.3 proteins per helix turn) around the RNA, which forms a hairpin loop structure (see the electron micrograph above). The structural organization of the virus gives stability.[13] The protein monomer consists of 158 amino acids which are assembled into four main alpha-helices, which are joined by a prominent loop proximal to the axis of the virion. Virions are ~300 nm in length and ~18 nm in diameter.[14] Negatively stained electron microphotographs show a distinct inner channel of radius ~2 nm. The RNA is located at a radius of ~4 nm and is protected from the action of cellular enzymes by the coat protein.[15] X-ray fiber diffraction structure of the intact virus was studied based on an electron density map at 3.6 Å resolution.[16] Inside the capsid helix, near the core, is the coiled RNA molecule, which is made up of 6,395 ±10 nucleotides.[17][18] The structure of the virus plays an important role in the recognition of the viral DNA. This happens due to the formation of an obligatory intermediate produced from a protein allows the virus to recognize a specific RNA hairpin structure.[19] The intermediate induces the nucleation of TMV self-assembly by binding with the hairpin structure.[20]

Genome

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Genome of tobacco mosaic virus

The TMV genome consists of a 6.3–6.5 kbp single-stranded (ss) RNA. The 3’-terminus has a tRNA-like structure, and the 5’-terminus has a methylated nucleotide cap. (m7G5’pppG).[21] The genome encodes 4 open reading frames (ORFs), two of which produce a single protein due to ribosomal readthrough of a leaky UAG stop codon. The 4 genes encode a replicase (with methyltransferase [MT] and RNA helicase [Hel] domains), an RNA-dependent RNA polymerase, a so-called movement protein (MP) and a capsid protein (CP).[22] The coding sequence starts with the first reading frame, which is 69 nucleotides away from the 5' end of the RNA.[23] The noncoding region at the 5' end can be varied in different individual virions, but there hasn't been any variation found between virions in the noncoding region at the 3' end.[24]

Physicochemicalreplication cycle in a plant pathogenic fungus,TMV is able to enter and replicate in cells of C. acutatum, C. clavatum, and C. theobromicola, which may not be an exception, although it has neither been found nor probably searched for in nature.[34]

Environment

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TMV is known as one of the most stable viruses. It has a very wide survival range. As long as the surrounding temperature remains below approximately 40 degrees Celsius, TMV can sustain its stable form. All it needs is a host to infect. If necessary, greenhouses and botanical gardens would provide the most favorable condition for TMV to spread out, due to the high population density of possible hosts and the constant temperature throughout the year. It also could be useful to culture TMV in vitro in sap because it can survive up to 3000 days.[35]