Poster: Heavy Metals

Abs # 110: Identification and characterization of Al tolerance genes in the Intermated B73xMo17 population of maize by QTL mapping

Presenter:	Hoekenga, Owen A, oah1@cornell.edu
Authors	Hoekenga, Owen A (A)   Mason, Paul  (A)   Shaff, Jon  (A)   Buckler, Ed  (B)   Kochian, Leon  (C)
Affiliations:	(A): Cornell University - Dept of Plant Biology (B): USDA-ARS/North Carolina State University (C): USDA-ARS/Cornell University

Aluminum (Al) is the third most abundant element in the earth’s crust and toxic to plant roots if solubilized at acidic pH. Aluminum toxicity, which results from inhibition of root growth and nutrient/water acquisition, is a serious limitation to crop production, as up to one-half of the world’s potentially arable land is acidic. Increasing plant aluminum tolerance has been an objective of plant breeders worldwide for many years, yet no tolerance genes have yet been cloned. The physiological mechanisms that underlie aluminum tolerance are somewhat better understood. The best-characterized mechanism involves an aluminum-activated release of low molecular weight di- and tri-carboxylic organic acids (e.g. malate, oxalate, citrate) that can bind soluble Al in the rhizosphere and prevent its uptake into the root. We initiated a quantitative trait loci analysis of aluminum tolerance in maize, using the IBM population as our subject, with the intention of identifying the genes responsible for tolerance to aluminum stress and the underlying physiological mechanisms. The IBM population is especially attractive as B73 and Mo17 utilize different tolerance processes to create similar levels of tolerance. Transgressive segregation has generated varieties with tolerance similar to that seen in elite aluminum tolerant materials developed by EMBRAPA Maize and Sorghum, far more tolerant than either parent. Using a preliminary dataset, we identified five QTL regions important for aluminum tolerance, where Mo17 contributes the superior allele for four loci. Interestingly, these four loci appear to act epistatically with one another suggesting they function in a common pathway.