After replication in the cytoplasm, viruses spread from the infected cell into the neighboring cells through plasmodesmata, membranous channels embedded by the cell wall. As obligate parasites, viruses have acquired the ability to utilize host factors that unwillingly cooperate for the viral infection process. For example, the viral movement proteins (MP) interacts with the host pectin methylesterase (PME) and both proteins cooperate to sustain the viral spread. However, how and where PMEs interact with MPs and how the PME/MP complexes favor the viral translocation is not well understood. Recently, we demonstrated that the overexpression of PME inhibitors (PMEIs) in tobacco and Arabidopsis plants limits the movement of Tobacco mosaic virus and Turnip vein clearing virus and reduces plant susceptibility to these viruses. Here we discuss how overexpression of PMEI may reduce tobamovirus spreading.
Keywords: CP, coat protein.; CW, cell wall; ER, Endoplasmic Reticulum; MP, movement protein; MeOH, methanol; PD, plasmodesmata; PM, Plasma membrane; PME, pectin methylesterase; PMEI, pectin methylesterase inhibitor; TMV, Tobacco mosaic virus; cell wall; methanol; pectin methylesterase; pectin methylesterase inhibitors; pectin methylesterification; plasmodesmata; virus spreading.