International Centre for Environmental Membrane Biology, Department of Horticulture, School of Food Science and Engineering, Foshan University, Foshan 528011, China.
Tasmanian Institute of Agriculture, University of Tasmania, Hobart, 7001, Australia.
Cells. 2022 Sep 2;11(17):2741. doi: 10.3390/cells11172741.
Arsenic (As) is a toxic metalloid for all living organisms and can cause serious harm to humans. Arsenic is also toxic to plants. To alleviate As toxicity, all living organisms (from prokaryotes to higher plants) have evolved comprehensive mechanisms to reduce cytosolic As concentration through the set of As transporters localized at the plasma and tonoplast membranes, which operate either in arsenite As(III) extrusion out of cells (via ArsB, ACR3, and aquaporins) or by sequestering arsenic into vacuoles (by ABC transporters). In addition, a special arsenate resistance mechanism found in some bacterial systems has evolved in an As hyperaccumulating fern , which involves transforming arsenate As(V) to an As(V) phosphoglycerate derivative by a glyceraldehyde 3-phosphate dehydrogenase and transporting this complex by an efflux transporter. In the present review, we summarize the evolution of these arsenic resistance mechanisms from prokaryotes to eukaryotes and discuss future approaches that could be utilized to better understand and improve As resistance mechanisms in plants.
砷(As)是所有生物的有毒类金属元素,会对人类造成严重危害。砷对植物也有毒性。为了减轻砷的毒性,所有生物(从原核生物到高等植物)都进化出了综合机制,通过位于质膜和液泡膜上的砷转运蛋白将细胞质中的砷浓度降低,这些机制要么通过将亚砷酸盐(III)(通过 ArsB、ACR3 和水通道蛋白)从细胞中排出,要么将砷螯合到液泡中(通过 ABC 转运蛋白)。此外,在一些细菌系统中发现的一种特殊的砷酸盐抗性机制在一些砷超积累蕨类植物中进化而来,其中涉及通过甘油醛 3-磷酸脱氢酶将砷酸盐(V)转化为砷酸盐(V)磷酸甘油酸衍生物,并通过外排转运蛋白运输该复合物。在本综述中,我们总结了这些砷抗性机制从原核生物到真核生物的进化,并讨论了未来可以利用的方法,以更好地理解和提高植物的砷抗性机制。