Research focus

​What are the mechanisms underlying differential distribution of the plant hormone auxin within plant tissues, and how do these processes regulate plant growth and architecture?

Plant development is characterized by a pronounced adaptability to different environmental conditions. Extensive post-embryonic development, involving the activity of permanent stem cell populations (meristems), de novo organ formation and changes in growth direction, provides plants with exceptional flexibility in terms of growth and survival. Differential distribution (gradients) of the plant signaling molecule auxin underlies many of these developmental events. These gradients are established and maintained by a directional, intercellular auxin transport called polar auxin transport. Polar auxin transport provides positional and directional information for many aspects of plant development.

Classical models postulate that polar auxin transport requires the activity of auxin influx and efflux carriers. Molecular genetic studies in the model plant Arabidopsis thaliana have identified AUX1/LAX and PIN gene families coding for components of influx and efflux carriers respectively. Studies in cultured plant, mammalian and yeast cells show that PINs mediate auxin efflux from cells. The PIN gene family in Arabidopsis consists of eight members, and orthologs have been found in most other plant species. Genetic studies have revealed the roles of the different PIN proteins in the establishment of auxin gradients mediating multiple developmental processes, including apical organogenesis and phyllotaxis, gravitropic and phototropic growth, root meristem patterning, vascular tissue development and embryonic axis formation.

The key feature of polar auxin transport, namely its controlled directionality, was postulated to result from the asymmetric, subcellular localization of the efflux carriers. Remarkably, as predicted, PIN proteins display an asymmetric localization within auxin transport competent cells and determine the direction of auxin flow. The decision on PIN polar targeting depends on their phosphorylation regulated by PINOID kinase and PP2AA phosphatase. As cellular levels (and thus the activity of PINOID) are dependent on auxin itself, this provides a possible feedback regulation between auxin and PIN polarity.
Polar targeting of PIN proteins is related to their continuous subcellular movement between endosomes and the plasma membrane. PIN internalization occurs by the clathrin-dependent endocytosis mechanism; its recycling back to the plasma membrane requires ARF GEF regulators of vesicle trafficking. The constitutive cycling of auxin transport components provides an entry point for internal and external signals, which in this manner can rapidly modulate PIN polarity. Dynamic changes of PIN polarity in response to environmental and developmental signals have been observed to divert auxin flow during gravitropic response, embryogenesis, post-embryonic organogenesis and tissue regeneration. In addition, auxin itself can influence the subcellular distribution of plasma membrane proteins, including PINs, by inhibiting their endocytosis, and thus regulate activity of its efflux.

These data show that PIN proteins are key components of an intricate auxin distribution network that mediates local auxin gradients in multiple developmental processes.
It also represents a unique model system to study the functional link between basic cellular processes, such as endocytosis or cell polarity establishment, and their developmental outcome at the level of the multi-cellular plant organism.