Hoekenga Owen A, Vision Todd J, Shaff Jon E, Monforte Antonio J, Lee Gung Pyo, Howell Stephen H, Kochian Leon V
Department of Plant Biology, Cornell University, Ithaca, New York 14853, USA.
Plant Physiol. 2003 Jun;132(2):936-48. doi: 10.1104/pp.103.023085. Epub 2003 Apr 24.
Aluminum (Al) toxicity, which is caused by the solubilization of Al3+ in acid soils resulting in inhibition of root growth and nutrient/water acquisition, is a serious limitation to crop production, because up to one-half of the world's potentially arable land is acidic. To date, however, no Al tolerance genes have yet been cloned. The physiological mechanisms of tolerance are somewhat better understood; the major documented mechanism involves the Al-activated release of Al-binding organic acids from the root tip, preventing uptake into the primary site of toxicity. In this study, a quantitative trait loci analysis of Al tolerance in Arabidopsis was conducted, which also correlated Al tolerance quantitative trait locus (QTL) with physiological mechanisms of tolerance. The analysis identified two major loci, which explain approximately 40% of the variance in Al tolerance observed among recombinant inbred lines derived from Landsberg erecta (sensitive) and Columbia (tolerant). We characterized the mechanism by which tolerance is achieved, and we found that the two QTL cosegregate with an Al-activated release of malate from Arabidopsis roots. Although only two of the QTL have been identified, malate release explains nearly all (95%) of the variation in Al tolerance in this population. Al tolerance in Landsberg erecta x Columbia is more complex genetically than physiologically, in that a number of genes underlie a single physiological mechanism involving root malate release. These findings have set the stage for the subsequent cloning of the genes responsible for the Al tolerance QTL, and a genomics-based cloning strategy and initial progress on this are also discussed.
铝(Al)毒性是作物生产的一个严重限制因素,因为全球多达一半的潜在耕地呈酸性。铝毒性是由酸性土壤中Al3+的溶解导致根系生长以及养分/水分吸收受到抑制所引起的。然而,迄今为止尚未克隆出耐铝基因。耐铝的生理机制在一定程度上得到了更好的理解;主要的记录机制涉及根尖中铝激活释放出与铝结合的有机酸,从而阻止铝吸收到毒性的主要作用位点。在本研究中,对拟南芥的耐铝性进行了数量性状基因座分析,该分析还将耐铝数量性状基因座(QTL)与耐铝生理机制相关联。分析确定了两个主要基因座,它们解释了从直立型兰茨贝格(敏感型)和哥伦比亚(耐受型)衍生的重组自交系中观察到的耐铝性变异的约40%。我们对实现耐铝性的机制进行了表征,发现这两个QTL与拟南芥根中铝激活释放苹果酸共分离。尽管仅鉴定出了两个QTL,但苹果酸释放几乎解释了该群体中耐铝性变异的全部(95%)。兰茨贝格直立型×哥伦比亚组合的耐铝性在遗传上比生理上更为复杂,因为涉及根苹果酸释放的单一生理机制有多个基因作为基础。这些发现为后续克隆负责耐铝QTL的基因奠定了基础,同时还讨论了基于基因组学的克隆策略及其初步进展。