B1L regulates lateral root development by exocytic vesicular trafficking-mediated polar auxin transport

Auxin and auxin-mediated signaling pathways involved in the regulation of lateral root development are well documented. Although exocytic vesicle trafficking plays an important role in auxin efflux carriers PIN recycling, and polar auxin transport during lateral root formation, however, the mechanistic details of these processes are not well understood. Here, we demonstrate that BYPASS1-LIKE (B1L) regulate lateral root development via exocytic vesicular trafficking-mediated polar auxin transport in Arabidopsis. In b1l mutants, the number of lateral roots increased significantly, and the phenotypes were mainly attributed to lateral root primordium initiation but not to the defects in lateral root primordium development. Furthermore, the auxin signal was stronger in the lateral root primordium of the b1l mutant at stage I than those observed in the wild-type (WT). Moreover, exogenous auxin and auxin transport inhibitory treatments indicated that the phenotype of lateral roots in b1l mutants can be attributed to higher auxin levels and that B1L regulates auxin efflux. Consistently, auxin efflux carriers PIN1-GFP and PIN3-GFP were expressed at higher levels in the lateral root primordium of the b1l mutants. Interestingly, we found that B1L interacted with the exocyst and b1l mutant showed a defect in PIN2 exocytosis. Finally, we found that B1L cooperated with EXO70B1 to regulate lateral root formation. Our findings reveal an essential regulatory mechanism of B1L that interacts with the exocyst to regulate PIN-mediated polar auxin transport and lateral root initiation.