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

Abstract

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 (<i>ise1</i> to <i>ise4</i>) or decreased (<i>dse1</i>) PD trafficking during embryogenesis. Despite their opposite effects on PD transport, we found that the transcriptional profiles of <i>dse1</i>, <i>ise3</i>, and <i>ise4</i> 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 <i>ise</i> versus <i>dse</i> 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.