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Polar transport-dependent local accumulation of auxin provides positional cues for multiple plant patterning processes. This directional auxin flow depends on the polar subcellular localization of the PIN auxin efflux regulators. Overexpression of the PINOID protein kinase induces a basal-to-apical shift in PIN localization, resulting in the loss of auxin gradients and strong defects in embryo and seedling roots. Conversely, pid loss of function induces an apical-to-basal shift in PIN1 polar targeting at the inflorescence apex, accompanied by defective organogenesis. Our results show that a PINOID-dependent binary switch controls PIN polarity and mediates changes in auxin flow to create local gradients for patterning processes.
The plant signaling molecule auxin plays a central role in a wide variety of development processes. A major determinant in auxin-mediated plant growth is the directed transport of auxin from foci of biosynthesis to sites of action. This polar auxin transport mediates vectorial gradients that underlie tropic growth responses and provide positional cues for apical-basal patterning, organogenesis, and vascular differentiation (1-4). The molecular characterization of the Arabidopsis thaliana pin-formed (pin1) mutant, which is defective in auxin transport and develops pin-like inflorescences, led to the identification of the PIN family of transporter-like membrane proteins. A substantial amount of data demonstrates that PIN proteins are important regulators of polar auxin transport that possibly function as auxin efflux carriers (4). PIN proteins display asymmetric subcellular localization at the plasma membrane, which determines the direction of polar auxin transport and thus establishes the local auxin gradients that influence different developmental processes. The polarity of PIN proteins can be rapidly modulated in response to external or developmental cues (1, 3, 5), a process that is enabled by continuous GNOM ARF GEF-dependent cycling of PINs between endosomes and the plasma membrane (6) (GNOM, Arabidopsis GNOM protein; ARF, ADP ribosylation factor; GEF, guanine nucleotide exchange factor).
Loss-of-function mutants of the protein serine-threonine kinase PINOID (PID) display apical organogenesis defects similar to those of the pin1 mutant (7). Constitutive overexpression of PID (35S::PID), but not of the kinase-negative MPID (35S::MPID), leads to hypocotyl and root agravitropy and to loss of the primary root meristem function (8, 9). The collapse of the root meristem in 35S::PID seedlings, which is characterized by the loss of meristem initials followed by terminal differentiation,...