Abstract
1.ABSTRACTLateral root growth occurs from primed xylem pole pericycle cells that can be specified as founder cells, but how these cells acquire the pluripotency state to initiate a root organogenesis program is not fully understood. Here, we find that the EMS 204 mutant is unable to specify founder cells due to a point mutation affecting the C-terminal HDS3 domain of the GNOM protein. We used genetics and cell biology to study the trafficking machinery of xylem pole pericycle cells, cells in which GNOM is primarily associated with recycling endosomes. We found that the lack of the HDS3 domain negatively affects the stability of the GNOM protein within the cells of the xylem pole pericycle and, subsequently, the integrity of the trafficking machinery of these cells. We determined that GNOM is responsible for the recycling of AUX1 toward the plasma membrane at the xylem pole pericycle and impairment of this recycling results in premature accumulation of AUX1 in the vacuole. In this work, we describe a cell type-specific cellular mechanism and the role of a particular domain during lateral root development.
Publisher
Cold Spring Harbor Laboratory