Plasmodesmal closure triggers stress responses

Changes in cellular connectivity is required for cell signaling, with elicitor-induced plasmodesmal closure and consequent cellular isolation required for a full immune response. To understand what occurs when plasmodesmal closure is initiated, we generated two inducible transgenic lines (LexA::PD-Plug and LexA::icals3m).

Inducing these genetic tools results in callose deposition at plasmodesmata, leading to plasmodesmal closure and cellular isolation, independent of a stimulus. We found that prolonged cellular isolation led to the upregulation of stress responsive genes and accumulation of salicylic acid, in addition to increased resistance to Pseudomonas syringae DC3000. We observed a more homogenous cellular isolation in LexA::icals3m lines in comparison to a heterogenous cellular isolation in LexA::PD-Plug, the latter which reflects more biological relevant observations in response stress elicitors.