Regulation of plasmodesmata by specialized metabolites glucosinolates in Arabidopsis thaliana

Communication is an essential component to all living organisms. In

plants, the additional cell wall surrounding each cell adds a layer of complexity

not observed in animals. To overcome the literal wall separating cells, plants

have evolved specialized pores to connect adjacent cells. Plasmodesmata (PD)

allow plants to have a continuous cytoplasm between cells. Although

plasmodesmata may appear simple and lack regulation, their structural

components and their regulatory machinery is complex and not well understood.

Organelle-to-nucleus-to-plasmodesmata signaling (ONPS) have been worked as

a leading model for a possible regulatory mechanism. Many of the details of

organelle-to-nucleus retrograde signaling pathways have been elucidated in

yeast, mammalian and plant model systems. Understanding mechanisms of

chloroplast-to-nucleus signaling will help elucidate the functions of retrograde

signaling in all organisms including bacteria and apicomplexans. Our previous

work with mutants lacking the chloroplast RNA helicase ISE2 indicates that

chloroplasts are important regulators of plant intercellular communication and

trafficking mediated by pores in the plant cell walls called plasmodesmata. Loss

of ISE2 has suggested defects in glucosinolates and in this dissertation we show

how glucosinolates can regulate intercellular trafficking via plasmodesmata. I

uncover the potential pathway of how the changes in the chloroplast by the loss

of ISE2 modulate nuclear signaling and ultimately disrupts the biosynthesis of

glucosinolates. I find that plants overexpressing ISE2 results in global

physiological defects that can partially be described as auxin defects. However, they are a more complex phenomenon. Further, I reveal that the addition of

glucosinolates alone to plants results in an increase in intercellular trafficking in a

dose-dependent manner.