Auxin is central to all aspects of plant growth and development from embryogenesis through senescence.   Auxin levels vary dramatically throughout the body and life of the plant, forming gradients that are a primary component of its action. Accordingly, plants have evolved intricate regulatory networks with considerable redundancy and adaptive plasticity to maintain auxin levels in response to changing environmental and developmental cues (Fig. 1).  We refer to this phenomenon as auxin homeostasis; specifically the biosynthesis, inactivation, transport, and inter-conversion pathways that regulate indole-3-acetic acid (IAA) levels.  Auxin response pathways are distinct from auxin homeostasis pathways; however, they clearly interact with each other and with other metabolic and signaling networks in the global process of auxin regulation.

Recent molecular and genetic studies in Arabidopsis have led to significant new insights into many aspects of auxin regulation including auxin biosynthesis, transport, metabolism and response.  Numerous pathways and gene families with direct roles in auxin regulation have been proposed, but there remain major gaps in our understanding of these networks.  Specifically, none of the proposed pathways are completely defined, their utilization throughout development is not well understood and even less is known about the mechanisms of pathway regulation and cross talk. Thus, more genes must be identified and many predicted to function in auxin regulation must be confirmed and assigned a developmental and physiological function.

We are particularly interested in understanding the impact of tryptophan (Trp) metabolism on auxin regulation and have developed several projects designed to address this issue.  One of these is summarized below:

Collaborative Research: Cellular and Subcellular Resolution of the Tryptophan-Related Pathways

A current research focus is on the interface between Trp primary and secondary metabolism.  Our goal is to determine at the cellular and subcellular level, the metabolic consequences of genetic disruption and dysregulation of Trp biosynthesis.  This goal will be accomplished by: 1) the development of methods for quantitative targeted metabolomics of indolic compounds, 2) the development of methods to achieve cellular and subcellular resolution in metabolite profiling; 3) targeted metabolite quantification of selected metabolites in Trp-dysregulated mutant lines at organ, cellular and subcellular resolution, and 4) the creation and analysis gene expression reporters for selected Trp metabolism genes and functional characterization of previously uncharacterized Trp biosynthetic genes (Target genes for 2010).