Nematodes, which feed on the root system of the plant, are another source of viral infection. In some cases, the virus is transferred from the invertebrate to the plant without growing in the vector. This is the case for Geminivirus transmission by white flies. Alternatively, viruses may replicate in both their invertebrate and plant hosts.
This is seen with tomato spotted wilt virus a plant bunya-virus and its thrip vector. In either case the viruses gain entry to cytoplasm of the plant host cell after the insect has begun to feed on plant tissue. Mechanical damage to the plant's cell wall also can be a means of entry for plant viruses. This approach is used most often in experimental settings when the leaf surface is scratched or abraded prior to inoculation with a virus suspension.
Therefore, it is likely that the plasmodesmata density may affect the induced resistance response to pathogen attack in plants. This idea was clarified when it was discovered that a protein, named PDLP5 plasmodesmata-located protein 5 , causes the production of salicylic acid, which enhances the defense response against plant pathogenic bacterial attack.
In , Eduard Tangl noticed the presence of the plasmodesmata within the symplasm, but it wasn't until when Eduard Strasburger named them plasmodesmata. Naturally, the introduction of the electron microscope allowed the plasmodesmata to be studied more closely.
In the s, scientists could study the movement of molecules through the plasmodesmata using fluorescent probes. However, our knowledge of plasmodesmata structure and function remains rudimentary, and more research needs to be performed before all is fully understood. Further research was long hindered because plasmodesmata are associated so closely with the cell wall. Scientists have attempted to remove the cell wall to characterize the chemical structure of the plasmodesmata. In , this was accomplished , and many receptor proteins were found and characterized.
Actively scan device characteristics for identification. Use precise geolocation data. Select personalised content. Create a personalised content profile. Measure ad performance. Select basic ads.
Create a personalised ads profile. Select personalised ads. Apply market research to generate audience insights. Measure content performance. Lipids provide the cohesion that keeps biological membranes intact. They spontaneously arrange themselves into a lipid bilayer because oily fat does not mix with water. The headgroups of one monolayer face an external aqueous solution, whereas the headgroups of the other monolayer face the interior of the cell.
Integral membrane proteins, such as viral fusion proteins, are inserted into the bilayer and project out from the lipid surface into the external solution-like icebergs. Membranes are able to fuse to each other because they are fluid 3 , and the lipids provide fluidity to the membrane.
Viruses initially stick to cell membranes through interactions unrelated to fusion proteins. The virus surfs along the fluid surface of the cell and eventually the viral fusion proteins bind to receptor molecules on the cell membrane 4.
If only binding occurred, the two membranes would remain distinct. Fusion does not happen spontaneously because bilayers are stable. Fusion proteins do the work of prodding lipids from their initial bilayer configuration. These proteins cause discontinuities in the bilayers that induce the lipids of one membrane e. Fusion proceeds in two major steps Fig. In the second step, the fusion proteins disrupt this single bilayer to create a pore that provides an aqueous pathway between the virus and the cell interior.
It is through this fusion pore that the viral genome gains entry into a cell and begins infection. The steps of fusion. Virus binds to specific receptors each illustrated as a small cactus on a cell membrane. Initially, four monolayers in blue separate the two interior aqueous compartments.
After fusion peptides insert into the target membrane, monolayers that face each other merge and clear from the merged region. The noncontacting monolayers bend into the cleared region and come into contact with each other, forming a new bilayer membrane known as a hemifusion diaphragm. At this point hemifusion , only two monolayers separate the compartments. The fusion protein acts as a nutcracker to force the formation of a pore within the hemifusion diaphragm.
This establishes continuity between the two aqueous compartments and fusion is complete. Hemifusion and pore formation appear to require comparable amounts of work, but the exact amount of energy needed for each step is not yet known 5. These energetic details may be important because the more work required to achieve a step, the easier it may be to pharmacologically block that step.
These energies are supplied by the viral fusion proteins, which are essentially molecular machines. Some of their parts move long distances during the steps of fusion.
Fusion proteins can be thought of as a complex assembly of wrenches, pliers, drills, and other mechanical tools. Because fusion is not spontaneous, discontinuities must be transiently created within the bilayer that allows water to reach the fatty, oily interior of the membrane.
Even a short-lived exposure of a small patch of the fatty interior to water is energetically costly. Similarly, creating a pore in a hemifusion diaphragm requires exposure of the bilayer interior to water 6. In contrast, pore enlargement needs no such exposure. Nevertheless, pore enlargement requires the most amount of work in the fusion process.
Energy is also needed because of another fundamental property of bilayer membranes. Biological membranes have shapes that are determined by their precise lipids and the proteins associated with them 7.
Work is required to force membranes out of their spontaneous shape, which is the shape of lowest energy. The fusion pore that connects the virus and cell is roughly an hourglass shape 8. The wall of a fusion pore is a membrane with components that are a mixture of the two original membranes. An hourglass shape deviates significantly from the spontaneous shape of the initial membranes that constitute the pore.
The greater the diameter of the pore, the greater is the area of the lining membrane, and so pore expansion is a highly energy consuming process. In fact, it appears that more energy is required for pore expansion than for hemifusion or pore formation.
All viral fusion proteins contain a greasy segment of amino acids, referred to as a fusion peptide or fusion loop. Soon after activation of the fusion protein, the fusion peptide inserts into the target membrane either plasma or endosomal.
At this point, two extended segments of amino acids are anchored to the membranes: the fusion peptides in the target membrane and the membrane-spanning domains of the fusion proteins in the viral envelope Fig. The fusion proteins continue to reconfigure, causing the two membrane-anchored domains to come toward each other. This pulls the viral envelope and cellular membrane closely together 9.
The fusion proteins exert additional forces, but exactly what these forces are and how they promote fusion remains unknown. A virion engulfed into an endosome is like a Trojan horse, because the cell perceives the virus particle as food. Fusion of viruses within endosomes depends critically on the acidic environment. Using purified HIS-tagged MPs as probes in a variety of assays Far Western assays, column filtration of plant protein extracts, screening of an Arabidopsis thaliana expression library and as probes for in situ localisation at LM and EM level , host proteins with affinity for viral MPs will be identified and characterised.
The outcome of this research will not only contribute to the understanding of virus movement, but will also give further insight in the host's cellular processes that are recruited by plant viruses. Successful infection of the host plant completely depends on the ability of progeny virus to move systemically from the initially infected cell into neighbouring cells and subsequently to other parts of the plant. Two clearly distinct events determine spread of virus through the plant: 1 movement of the virus from cell-to-cell through plasmodesmata to the vascular tissue and 2 transport of the virus over long distances through the vascular system to other plant parts.
For local cell-to-cell transport plant viruses encode a so-called "movement protein" and the principles for this process, involving passage of virus-modified plasmodesmata, have been elucidated for our model virus, Cowpea mosaic virus CPMV.
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