Abstract
The auxin distribution is established by polar auxin transport that is dependent on polar-localized auxin efflux carriers, PIN-FORMED (PIN). Recently, a NONPHOTOTROPHIC HYPOCOTYL 3 (NPH3)-like protein, MACCHI-BOU 4 (MAB4), has been reported to regulate polar auxin transport through the control of subcelluar localization of PIN1 proteins in cotyledon development. MAB4 has four homologs, named MAB4/ENP LIKE 1 (MEL1), MEL2, MEL3 and MEL4. In root tips of mel1 mel2 mel3 mel4 quadruple mutants, PIN2 abundance was severely reduced and PIN2 polarization was weakened. To investigate the mechanism by which the MAB4 subfamily genes regulate PIN2 localization, we used pharmacological approaches in PIN2-GFP expressing mutants. When treated with BFA or wortmannin, PIN2 protein accumulated in induced intracellular compartments of mel1 mel2 mel3 mel4 roots as well as wild-type roots. Meanwhile, when treated with thyrphostin A23 that is a blocker for clathrin-dependent endocytosis, PIN2 internalization was not blocked in mel1 mel2 mel3 mel4 roots. These results suggest that the MAB4 subfamily genes regulate PIN endocytosis in the plasma membrane.
