Arabidopsis lipid kinase FAB1 regulates lateral root emergence via clathrin-mediated endocytosis of PIN-FORMED 3.

Abstract

Lateral root (LR) growth enables plants to explore regions of the soil, anchor themselves, and optimize nutrient and water uptake. LR development is characterized by the establishment of an auxin maximum at the lateral root primordium (LRP); however, the regulatory mechanisms underlying this process remain poorly understood. In Arabidopsis (Arabidopsis thaliana), FORMATION OF APLOID AND BINUCLEATE CELLS1 (FAB1) encodes a lipid kinase responsible for biosynthesizing phosphatidylinositol 3,5-bisphosphate. Our findings show that auxin induces FAB1 expression through AUXIN RESPONSE FACTOR7/19 (ARF7/19). In turn, FAB1 modulates the auxin maximum at the LRP tip by regulating clathrin-mediated endocytosis of the PIN-FORMED (PIN) auxin efflux carriers, forming a previously uncharacterized auxin-induced feedback loop during LR development. Loss of FAB1 function markedly increases LR number, while FAB1 overexpression suppresses LR formation. Diminished FAB1 activity leads to less clathrin accumulation at the plasma membrane (PM), limited endocytosis, and greater PIN3 retention at the LRP PM, thereby enhancing auxin flow toward LRP tips and promoting emergence. These results identify FAB1 as a negative regulator of lateral root development that fine-tunes auxin transport to facilitate organ emergence.