Abstract
Polar auxin transport is mainly dependent on the activity of auxin efflux carriers, PIN-FORMED (PIN) proteins, localized in the plasma membrane with polarity. However, molecular mechanisms for the establishment of sequential PIN polarity remain to be uncovered. Recently, a NPH3-like protein MACCHI-BOU (MAB) 4 has been reported to regulate polar auxin transport through the control of PIN localization in organ formation. This time, we analyzed the role of MAB4/ENP-LIKE (MEL) 1-4, homologous to MAB4, in the establishment of PIN polarity. mel1 and mel2 mutations enhanced mab4 mutant phenotypes as mab4 mel1 mel2 triple mutants developed pin-like inflorescences. In addition, mel1 mel2 mel3 mel4 quadruple mutants displayed severe defects in the root gravitropism. In these mutants, the abundance of polar localized PIN protein was severely reduced with weakening in PIN polarity. Furthermore, MAB4 and all MEL proteins were mainly localized close to the plasma membrane with polarity. MAB4 and MEL polarity was almost identical to PIN polarity. These results suggest that MEL genes regulate auxin-related morphogenesis through the control of PIN localization redundantly with MAB4.
