Many plant viruses encode for a protein(s) that is essential for movement from the site of replication to surrounding, uninfected cells. These proteins have the ability to interact with endogenous plasmodesmal proteins to increase the plasmodesmal size exclusion limit (SEL). When expressed in transgenic tobacco plants, the movement protein of tobacco mosaic virus (TMV-MP), in addition to increasing the SEL, also alters the biomass partitioning and carbon allocation within these plants. During the day, source leaves of transgenic plants that express the TMV-MP accumulate sugars and starch and biomass partitioning into root tissue is reduced when compared with vector control plants. However, studies with transgenic tobacco plants expressing various mutant forms of the TMV-MP, as well as plants expressing the MP of cucumber mosaic virus, established that the effect on biomass partitioning and carbon allocation is independent of its effect on plasmodesmal SEL. Graft experiments and analysis of transgenic tobacco and potato plants expressing the TMV-MP under tissue-specific promoters indicated that mesophyll cells may be the site of TMV-MP action. In the light of these results and evidence that plasmodesmata are capable of trafficking macromolecules, it is proposed that plasmodesmata within the leaf establish a special communication network between the companion cells (CC) and the mesophyll. In this model, output signals from the CC to the mesophyll and input signals from the mesophyll to the CC are involved in regulating photosynthesis occurring within the mesophyll and loading/export that takes place in the CC-SE complex. It is proposed that the TMV-MP-mediated influence on plasmodesmal trafficking of these signal molecules alters this endogenous control mechanism resulting in a shift in biomass partitioning and carbon allocation.

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