Glucose-TOR-PDCB signaling restricts cell-to-cell communication through callose deposition.

Plant cells are connected by plasmodesmata (PD), membrane-lined channels that facilitate cell-to-cell transport. Forward genetic screens to uncover regulators of PD transport identified mutants with increased (ise1 to ise4) or decreased (dse1) PD trafficking during embryogenesis. Despite their opposite effects on PD transport, we found that the transcriptional profiles of dse1, ise3, and ise4 were notably similar with one notable exception: the set of genes controlled by the conserved kinase TARGET OF RAPAMYCIN (TOR) and ABI5, a bZIP transcription factor that acts downstream of TOR. We then showed that the glucose-TOR-ABI5 signaling axis regulates PD transport by driving expression of PD-localized callose binding proteins (PDCBs), which are oppositely regulated in ise versus dse mutants and promote callose deposition at PD. Together, this study establishes a mechanism for metabolic regulation of cell-to-cell transport by TOR-ABI5-PDCB signaling.