Systemic infection in plants requires viruses to navigate the complex physiological barriers of the phloem. While cell-to-cell movement is mediated by movement proteins (MPs), long-distance movement has traditionally been viewed as a function of the coat protein (CP), often linked to the assembly of mature virions. However, an emerging body of evidence suggests that the boundary between these modules is less rigid than previously assumed. Here, we first outline the major vascular checkpoints that can act as bottlenecks for longdistance movement, and then summarize experimental contexts in which virion assembly and systemic spread can be decoupled. Finally, we examine structural and evolutionary connections between single jelly-roll CPs and the 30K superfamily of MPs, highlighting how a shared fold may enable partial functional overlap that can lessen CP dependence during long-distance transport. By integrating "unorthodox" examples, we aim to provide a framework for interpreting CP dependence as an outcome shaped by the dominant constraints at phloem interfaces.
Jung et al. (2026) studied this question.