Genome-wide association mapping identifies a new arsenate reductase enzyme critical for limiting arsenic accumulation in plants.
Genome-wide association mapping identifies a new arsenate reductase enzyme critical for limiting arsenic accumulation in plants.
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DOI:
10.1371/journal.pbio.1002009
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发表时间:
2014-12
期刊:
影响因子:
9.8
通讯作者:
Salt DE
中科院分区:
文献类型:
--
作者:
Chao DY;Chen Y;Chen J;Shi S;Chen Z;Wang C;Danku JM;Zhao FJ;Salt DE
A genome-wide association study identifies the enzyme in plants that transforms arsenate into arsenite, allowing its extrusion into the soil and thereby controlling arsenic accumulation. Inorganic arsenic is a carcinogen, and its ingestion through foods such as rice presents a significant risk to human health. Plants chemically reduce arsenate to arsenite. Using genome-wide association (GWA) mapping of loci controlling natural variation in arsenic accumulation in Arabidopsis thaliana allowed us to identify the arsenate reductase required for this reduction, which we named High Arsenic Content 1 (HAC1). Complementation verified the identity of HAC1, and expression in Escherichia coli lacking a functional arsenate reductase confirmed the arsenate reductase activity of HAC1. The HAC1 protein accumulates in the epidermis, the outer cell layer of the root, and also in the pericycle cells surrounding the central vascular tissue. Plants lacking HAC1 lose their ability to efflux arsenite from roots, leading to both increased transport of arsenic into the central vascular tissue and on into the shoot. HAC1 therefore functions to reduce arsenate to arsenite in the outer cell layer of the root, facilitating efflux of arsenic as arsenite back into the soil to limit both its accumulation in the root and transport to the shoot. Arsenate reduction by HAC1 in the pericycle may play a role in limiting arsenic loading into the xylem. Loss of HAC1-encoded arsenic reduction leads to a significant increase in arsenic accumulation in shoots, causing an increased sensitivity to arsenate toxicity. We also confirmed the previous observation that the ACR2 arsenate reductase in A. thaliana plays no detectable role in arsenic metabolism. Furthermore, ACR2 does not interact epistatically with HAC1, since arsenic metabolism in the acr2 hac1 double mutant is disrupted in an identical manner to that described for the hac1 single mutant. Our identification of HAC1 and its associated natural variation provides an important new resource for the development of low arsenic-containing food such as rice. Arsenic is a human carcinogen that accumulates from soil into many different food crops, where it presents a significantly increased cancer risk when foods derived from these crops are consumed. Plants naturally control the amount of arsenic they accumulate by first chemically converting arsenate into arsenite, which is then extruded from the roots back into the soil. Because arsenate is a chemical analogue of phosphate, conversion of arsenate in the root to arsenite may also prevent arsenic being efficiently transported to the shoots via the phosphate transport system. The chemical reduction of arsenate to generate arsenite is therefore clearly a key component of a plant's detoxification strategy. Here, we use genetic methods to identify the enzyme responsible for this crucial reaction—HAC1. We show that HAC1 is responsible for arsenate reductase activity in both the outer layer of the root (epidermis) and the inner layer adjacent to the xylem (pericycle). In its absence, the roots return less arsenic to the soil and the shoots accumulate up to 300 times more arsenic. This knowledge creates new opportunities to limit arsenic accumulation in food crops, thereby helping to reduce the cancer risk from this food-chain contaminant.
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影响因子:
4.5
作者:
Baxter I;Brazelton JN;Yu D;Huang YS;Lahner B;Yakubova E;Li Y;Bergelson J;Borevitz JO;Nordborg M;Vitek O;Salt DE
通讯作者:
Salt DE
影响因子:
3.8
作者:
Gregus, Zoltan;Roos, Goedele;Nemeti, Balazs
通讯作者:
Nemeti, Balazs
DOI:
10.1111/j.1469-8137.2011.03789.x
发表时间:
2011-10
期刊:
The New phytologist
影响因子:
--
作者:
Carey AM;Norton GJ;Deacon C;Scheckel KG;Lombi E;Punshon T;Guerinot ML;Lanzirotti A;Newville M;Choi Y;Price AH;Meharg AA
通讯作者:
Meharg AA
影响因子:
4.5
作者:
Chao DY;Silva A;Baxter I;Huang YS;Nordborg M;Danku J;Lahner B;Yakubova E;Salt DE
通讯作者:
Salt DE
影响因子:
4.5
作者:
Filiault DL;Maloof JN
通讯作者:
Maloof JN