|Stephens, Brian - UNIV CALIF-DAVIS|
|Cook, Douglas - UNIV CALIF-DAVIS|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: February 12, 2007
Publication Date: May 24, 2007
Citation: Stephens, B.W., Cook, D.R., Grusak, M.A. 2007. MtZIP1: A divalent metal transporter from the model legume Medicago truncatula [abstract]. In: Zinc Crops 2007, May 24-26, 2007, Istanbul, Turkey. Poster GMB-7. Technical Abstract: Micronutrients such as zinc, copper, iron, and manganese are essential for the efficient functioning of a variety of proteins involved in various plant biological processes. The plant must regulate the uptake of these metals, since either too low or high a concentration of metals in the plant will be detrimental. To achieve this balance, plants utilize and regulate the expression of several types of micronutrient transporters, including those of the ZIP family of divalent metal transporters. In the model legume, Medicago truncatula, seven ZIP genes have been identified, with three of these protein products (MtZIP1, MtZIP5, and MtZIP6) showing an ability to transport Zn (based on yeast complementation studies). We are characterizing the ZIP proteins in Medicago to achieve a better understanding of Zn uptake from the rhizosphere and partitioning within the plant. In addition, we have identified an MtZIP1 mutant that we are using to characterize whole-plant Zn dynamics. Zinc transport studies have confirmed that MtZIP5 and MtZIP6 are high affinity transporters with Km's around 0.4 uM and Vmax values around 1 pmol/min/10^6 cells. MtZIP1, on the other hand, is a low affinity transporter with a Km of 1.5 uM and Vmax of 8 pmol/min/10^6 cells. The higher values for MtZIP1 suggest that it has a role in the internal transport of zinc within the plant, rather than being involved in uptake from the rhizosphere. MtZIP5 and MtZIP6 may be involved both in root uptake of Zn, as well as internal transport. A mutation in MtZIP1 was identified during the screening of a TILLING population. The mutant allele had a deletion at base pair 27 of the first exon, which resulted in the insertion of a stop codon. The growth characteristics of the mutant are similar to wild-type A17 for the first several weeks. However, the mutants then show decreased growth, with internodes that are shorter than those of A17. Mutant plants have to be supplemented with zinc by foliar spray to partially relieve the effects of the mutation. Radiotracer studies showed that the MtZIP1 mutant partitions less of its absorbed Zn to shoots, relative to wild-type plants. These results suggest that MtZIP1 functions somewhere between the site of Zn absorption at the root epidermis and the point of Zn entry into the xylem pathway (prior to subsequent root to shoot translocation).