Volume 9, Issue 1, Pages 46-56 (January 2016) Integrating Hormone- and Micromolecule-Mediated Signaling with Plasmodesmal Communication  Xiao Han, Jae-Yean Kim  Molecular Plant  Volume 9, Issue 1, Pages 46-56 (January 2016) DOI: 10.1016/j.molp.2015.08.015 Copyright © 2016 The Author Terms and Conditions

Figure 1 Hypotheses for Phloem-Loading Regulation Mediated by Plasmodesmal Control in Companion Cells of Wild-type (A), tie-dyed (B) and GSD1ox (C). WT, wild-type; tdy, tie-dyed2; GSD1ox, GSD1 overexpressor. VP, vascular parenchima; CC, companion cell; SE, sieve element. Compared with the wild-type, tdy2 and GSD1ox show defective phloem unloading caused by either open plasmodesmata or closed plasmodesmata in companion cells. Thick arrows and thin arrows indicate high and low flux of sucrose, respectively. Question mark (?) indicates a hypothetical involvement of oil bodies in reduced sucrose movement into SE. Molecular Plant 2016 9, 46-56DOI: (10.1016/j.molp.2015.08.015) Copyright © 2016 The Author Terms and Conditions

Figure 2 ROS-Mediated Plasmodesmal Modulation. Organelle redox states differentially regulate PD. The suppression or mutation of ISE1, ISE2, or GAT1, or treatment with salicylhydroxamic acid or paraquat, modulates plasmodesmal permeability. This can be achieved by callose-dependent or callose-independent processes. Reduced plastid and oxidized mitochondrion modified the structure of primary PD into secondary PD to increase permeability. Oxidized plastid induced callose accumulation at PD to reduce permeability. Green, endoplasmic reticulum; blue, cell wall. Molecular Plant 2016 9, 46-56DOI: (10.1016/j.molp.2015.08.015) Copyright © 2016 The Author Terms and Conditions

Figure 3 Callose Mediates Feedback Loop for Intercellular Signaling through PD. Hormone (Auxin, SA, CK, and GA) signaling is activated via ARFs, PDLP5, or unknown factors, and then control PD permeability through callose-dependent and/or callose-independent pathways. Callose synthases and β-1,3-glucanases are key factors that control the callose-dependent pathway. Chitin-mediated LYM2 activation and sterol deficiency in PD lipid raft increase callose deposition through activation of callose synthesis and inactivation of callose degradation, respectively. ROS controls both callose-dependent and callose-independent pathways, as shown in Figure 2. Auxin activates the ARF7-GSL8 positive feedback loop that restricts auxin movement through PD (blue lines). Different colors indicate diverse signaling from micromolecules. CK, cytokinin; SA, salicylic acid; GA, gibberellic acid; ROS, reactive oxygen species; ARF, AUXIN RESPONSE FACTOR. Question marks (?) indicate unidentified factors. Molecular Plant 2016 9, 46-56DOI: (10.1016/j.molp.2015.08.015) Copyright © 2016 The Author Terms and Conditions