NASCArrays Information at The BAR

Welcome to NASCArrays information at the BAR. This page hosts meta-information from the NASCArrays service (2002-2013). This information was parsed from text files available on the NASCArrays site. NASCArrays data is on iPlant server. To download experiment data from iPlant, please click on the experiment number. To download the CEL files, please click on the ftp link.

Experiment:225
Title:RESPONSE TO IRON DEFICIENCY.
Date:2005-03-11
Description:Rationale: We would like to arrive at a molecular understanding of iron uptake in plants and to determine how cellular iron status may regulate the uptake, storage and utilization of iron. Understanding iron uptake in plants is important as one-third of the world's soils are iron deficient. Furthermore, iron deficiency in humans is the most prevalent nutritional problem in the world today, affecting an estimated 2.7 billion people. Iron deficiency, along with deficiencies of the micronutrients vitamin A and iodine, are often referred to as 'hidden hunger.' Clearly, we need to understand how plants acquire iron, both from the point of view of improving plant growth and crop yields and for improving human nutrition. Food-based solutions to 'hidden hunger' offer sustainable solutions to problems of malnutrition. For most of the world, plant material is the major source of iron so any progress we can make to ensure plants have higher stores of bio-available iron will go a long way towards solving an important problem in human nutrition. Experiment: We will compare the pattern of gene expression in roots of wild type plants (ecotype Columbia) grown under iron-sufficient conditions to that of roots from plants grown under iron-deficient conditions. We expect to identify 3 classes of genes: those which display up-regulation, down regulation, or those whose expression remains unchanged. We know that a number of genes are transcriptionally responsive to iron availability, including those encoding a Fe(III) chelate reductase (FRO2), a specific isoform of a H+-ATPase (AHA2), and an iron transporter (IRT1). Expression of all three genes is induced in roots under iron deficiency. We would also like to look at patterns of gene expression in roots of frd3 mutants grown with and without iron. frd3 mutants express Fe(III) reductase activity under both iron-deficient and iron-sufficient conditions, unlike wild type plants. They also show constitutive expression of IRT1. Despite having de-regulated iron deficiency responses, frd3 phenotypically resembles an iron-deficient plant i.e. it is chlorotic. Taken together, these data suggest that FRD3 may be a regulatory gene. The ability to determine whether the expression of other iron-regulated genes is also affected in a frd3 mutant should allow us to initially focus on a smaller number of genes than we anticipate will be identified in the experiment using wild type plants grown with and without iron.
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