Plasmodesmata enable the trafficking of various signaling molecules, as well as viruses that exploit these channels for their intercellular movement. Viral movement relies on the endoplasmic reticulum (ER), which serves as a stable platform for the assembly of viral replication complexes and their subsequent shuttling toward plasmodesmata. The role of the ER in the intercellular movement of endogenous proteins is less clear. In the root meristem, the mobile transcription factor SHORT-ROOT (SHR) traffics between cell layers to regulate root radial patterning and differentiation. Movement of SHR is a regulated process that requires several cellular factors including the endomembrane system, intact microtubules and an endosome-associated protein named SHR-interacting-embryonic-lethal (SIEL). Recently, we found that KINESIN G (KinG) interacts with both SIEL and microtubules to support the cell-to-cell movement of SHR. Here, we provide evidence that both SHR-associated endosomes and KinG localize to the endoplasmic reticulum (ER) and that movement of SHR-associated endosomes occurs on the ER. Moreover, we show that compromised ER structure leads to a reduction in the cell-to-cell movement of SHR. Collectively, these results support the hypothesis that the ER plays a role in SHR movement.
Keywords: Cell-to-cell movement; Endoplasmic reticulum; Golgi movement 8; Intercellular trafficking; Kinesin G; Plasmodesmata; SHORT-ROOT; Synaptotagmin a.