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.