Abstract
During their evolution, viruses acquired genes encoding movement protein(s) (MPs) that mediate the intracellular transport of viral genetic material to plasmodesmata (Pd) and initiate the mechanisms leading to the increase in plasmodesmal permeability. Although the current view on the role of the viral MPs was primarily formed through studies on tobacco mosaic virus (TMV), the function of its MP has not been fully elucidated. Given the intercellular movement of MPs independent of genomic viral RNA (vRNA), this characteristic may induce favorable conditions ahead of the infection front for the accelerated movement of the vRNA (i.e. the MP plays a role as a “conditioner” of viral intercellular spread). This idea is supported by (a) the synthesis of MP from genomic vRNA early in infection, (b) the Pd opening and the MP transfer to neighboring cells without formation of the viral replication complex (VRC), and (c) the MP-mediated movement of VRCs beyond the primary infected cell. Here, we will consider findings that favor the TMV MP as a “conditioner” of enhanced intercellular virus movement. In addition, we will discuss the mechanism by which TMV MP opens Pd for extraordinary transport of macromolecules. Although there is no evidence showing direct effects of TMV MP on Pd leading to their dilatation, recent findings indicate that MPs exert their influence indirectly by modulating Pd external and structural macromolecules such as callose and Pd-associated proteins. In explaining this phenomenon, we will propose a mechanism for TMV MP functioning as a conditioner for virus movement.
Highlights
Since viral molecules are too large for passive transport through plasmodesmata (Pd) by diffusion, viral genomes during evolution acquired genes encoding specific proteins that can induce plasmodesmal dilation
The second mechanism suggested that movement protein(s) (MPs) did not affect Pd but rather stimulated cellular mechanisms to overcome the resistance of plant cells to the virus and allow intercellular spread
It must be borne in mind that mechanical trauma and damage to the cell wall, which are a prerequisite for the virus to enter cells, causes the immediate release of methanol generated by both pre-existing in the cell wall pectin methylesterase (PME) and newly synthesized one (Dorokhov et al, 2012)
Summary
Since viral molecules are too large for passive transport through plasmodesmata (Pd) by diffusion, viral genomes during evolution acquired genes encoding specific proteins that can induce plasmodesmal dilation. The introduction of the tobacco GLU I gene encoding BG into the TMV genome led to an increase in the local lesion size, which confirms the role of BG as a callose-hydrolyzing enzyme in the cell-to-cell movement of viruses (Bucher et al, 2001) It must be borne in mind that mechanical trauma and damage to the cell wall, which are a prerequisite for the virus to enter cells, causes the immediate release of methanol generated by both pre-existing in the cell wall pectin methylesterase (PME) and newly synthesized one (Dorokhov et al, 2012). Since MP was shown to have RNAbinding properties (Citovsky et al, 1990) and to inhibit its own FIGURE 2 | Possible mechanisms of cell conditioning by nonviral factors induced by cell wall trauma and the specific effects of virus-directed MP, leading to the creation of favorable conditions for the intercellular spread of infection.
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