Uncovering the mechanisms of secondary plasmodesmata formation and virus mediated changes in intercellular trafficking

Intercellular communication is critical for all life on earth. From quorum sensing in bacteria to the electrical signals controlling our every move, the ability to share and exchange information with our neighbors is critical for growth and development. In plants, this communication can be achieved through two major pathways, apoplastic signaling or symplastic signaling through membrane lined pores in the cell wall called plasmodesmata. These pores form cytoplasmic bridges between neighboring cells and are used to traffic nutrients and signaling molecules throughout the plant. They also form direct routes for plant pathogens to rapidly spread throughout the plant. Plant viruses are particularly well adapted to take advantage of these intercellular connections. During virus infection, trafficking through plasmodesmata increases in a phenomenon known as gating. The long standing interpretation of this increase in trafficking has been that it allows for rapid spread of the virus into neighboring, uninfected tissues. While the plasmodesmata-virus relationship has been studied extensively and has provided many insights into the functioning and regulation of these small pores, the changes that occur during infection to increase the trafficking remain unknown. The results presented in this dissertation demonstrate that the observed increase intercellular trafficking is the result virus-induced formation of new plasmodesmata. Using this system, details of the mechanisms behind the cell biology of plasmodesmata formation are revealed. Using the data presented here, new models for gating during virus infection and secondary plasmodesmata formation are proposed.