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United States Department of Agriculture

Agricultural Research Service

Title: The Basis of Aluminum Tolerance Encoded by the Alt3 Locus of Rye

Authors
item Collins, Nicholas - UNIV OF ADELAIDE, S. AUS.
item Gustafson, J

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: September 15, 2007
Publication Date: October 20, 2007
Citation: Collins, N., Gustafson, J.P. 2007. The Basis of Aluminum Tolerance Encoded by the Alt3 Locus of Rye [abstract]. 2007 Genomics Symposium: The Genomics of Drought, October 2007, Adelaide, South Australia. Paper No. 6.

Interpretive Summary: It is clear that many of the world’s farmers living on marginal soils, which possess properties (such as high acidity) that offer a stressful environment for plant growth, do not have the management options required to improve wheat yields. Aluminium, the most abundant metal on earth, is highly toxic to plant growth and is found in about 2.5 billion hectares of acid soils, including several million in the United States. Therefore, the development of wheat cultivars capable of improved production on marginal and stressful soils is needed. The present study was designed to characterize the location of gene complexes controlling aluminium tolerance in rye and to establish how they function to make rye the most tolerant of all the cereals to aluminium toxicity. The study involved the analysis of the inheritance of aluminium tolerance in rye, utilizing a rye segregating population, and in wheat by growing seedlings in a hydroponic solution containing aluminium and measuring root growth. The study clearly demonstrated that in rye there are multiple copies of several genes families conferring tolerance to soils high in aluminium, while wheat appears to contain only one copy of a single gene family. These results are important in our understanding of why rye is significantly more tolerant to production on acid soils than is wheat. We now have characterized the gene complexes controlling aluminium tolerance in rye, and have formulated approaches to improving the aluminium tolerance of wheat by either manipulating the rye gene complex into wheat, or by increasing the number of copies of the aluminium tolerance gene currently existing in wheat.

Technical Abstract: Aluminium (Al) toxicity, affecting around half of the world’s arable land, severely hinders the ability of crop plants to cope with drought and nutrient stresses by restricting root growth and function. Among the cultivated cereals, rye is the most Al tolerant. At the Alt3 Al tolerance locus on rye 7RS, there is a cluster of genes homologous to the known Almt1 malate transporter and Al tolerance gene of wheat. This contrasts with wheat, in which only one Almt1 gene copy at the tolerance locus has been described. There are 5 copies in the tolerant rye mapping parent and 2 in the intolerant parent. Fine genetic mapping essentially excluded all other types of genes flanking the cluster as possibly providing the Alt3 tolerance, including a nearby homologue of a MATE transporter gene proposed to control Al tolerance and citrate secretion in barley. Two of the recombination events occurred within the cluster, one of which gave rise to a new hybrid gene (and novel-sequence protein) that is functional in providing tolerance. Expression analysis of individual Almt1 gene family members identified which members were expressed in the root tip and leaves and induced by Al stress. Although one Almt1 gene is highly transcribed in root tips of the intolerant parent, a MITE transposable element present in one of its introns appears to causes inefficient mRNA splicing, which may explain why this gene is unable to provide full tolerance. The ability of the rye Almt1 proteins to transport different Al-detoxifying organic acids in to the soil was studied using enzymatic assays of root exudates of recombinant lines. We are currently extending this investigation by using full metabolite profiling of root exudates and electrophysiological studies of Almt1-expressing frog oocytes.

Last Modified: 12/28/2014
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