Grant: Discovery Grants Program - Individual

Our work strives to understand the molecular mechanisms controlling vein formation. The vascular system is fundamental to plant structure and function, providing a skeleton and efficient transport routes for water, photosynthates, essential nutrients, pathogens and signaling compounds. Thus, our findings may impact plant modifications designed to produce more wood, withstand drought stress, or improve photosynthetic capacity. The factors identified as being important to vein formation are primarily involved in transport of or response to the plant hormone, auxin. Auxin is fundamental to a huge number of plant developmental processes, including embryo polarity, root organization, placement of branch roots and leaves and response to gravity and light. In all processes directional auxin transport through asymmetric placement of auxin influx and efflux proteins on cell membranes is critical to auxin function. While control of auxin efflux is increasingly well understood, little is known about the control of auxin influx. Vein pattern seems to be sufficiently complex that screens for vein pattern mutants reveal novel components in auxin transport and response, with either redundant roles or effects too subtle to be detected in classical screens. Thus, beyond providing a better understanding of vascular formation, our work will reveal molecular mechanisms controlling auxin localization and activity throughout plant development. We propose to dissect the role of four genes - AUTOBAHN (ABN), FORKED1 (FKD1), UNHINGED (UNH) and GRASSY (GSY) - identified by mutation. Plants mutant in ABN make highly disordered veins and alter placement of leaves. Our data suggest that these plants are defective in auxin influx, and thus represent the first mutation that links auxin influx to leaf position and vein pattern. We plan experiments to find out what product ABN makes, and how it influences auxin influx. The FKD1 gene product is a protein with a domain indicative of involvement in properly localizing the auxin efflux protein to the cell membrane. We will test this idea. Finally, we will identify and characterize both UNH and GSY whose mutant phenotypes suggest a role in auxin transport or signaling.