Redox homeostasis regulates plasmodesmal communication in Arabidopsis meristems.

Cell-to-cell communication is crucial for multicellular development, and in plants occurs through specialized channels called plasmodesmata (PD). In our recent manuscript we reported the characterization of a PD trafficking mutant, 'gfp arrested trafficking 1' (gat1), which carries a mutation in the thioredoxin-m3 (TRX-m3) gene. gat1 mutants showed restricted GFP transport from the phloem to the root meristem that appears to result from structural modifications in the PD channel. We found accumulation of reactive oxygen species (ROS) and callose, as well as a reduction in starch granules in the gat1 root meristem. Application of oxidants to wildtype plants and expression of our GFP reporter in the mutant root meristemless 1 (rml1) mimic the gat1 phenotype. Our results suggest that mutations in GAT1 cause ROS accumulation and induce the biosynthesis of callose, which in turn block PD transport. Therefore, we propose a model whereby GAT1/TRX-m3 is a component of a redox-regulated pathway that maintains PD permeability in Arabidopsis meristems.