S-亚硝基谷胱甘肽还原酶在植物应答镉胁迫中的作用机制

Cadmium (Cd) contamination of agricultural soils is an increasingly serious problem in China. Molecular breeding non-food crops with higher capacities of Cd accumulation and resistance, and using them for remediation of the contaminated soil, are recognized as an inexpensive and effective strategy. The breeding of these crops requires understanding the mechanisms that are involved in Cd uptake and resistance of plants. However, the information on these mechanisms is still limited so far. Nitric oxide (NO) plays important roles in regulating Cd uptake and resistance of plants. It has been shown that Cd stress significantly inhibited the activity of S-nitrosoglutathione reductase (GSNOR) which is involved in controlling cellular NO level. Our preliminary study found that loss the function of GSNOR in Arabidopsis plants not only leads to increased Cd accumulation, but also enhances Cd resistance. Considering the potential linkage between the Cd stress, GSNOR and NO, this project will investigate the behavior of GSNOR in response to Cd stress and its role in mediating Cd-induced NO accumulation by using Arabidopsis plants. In addition, based on the analysis of the gene expressions and protein modifications which are involved in Cd uptake and resistance, we will also emphasize to comprehensively investigate how the inhibition of GSNOR activity and the elevation of NO level regulate the uptake of Cd by roots, immobilization of Cd by cell wall and resistance of cellular oxidative stress. These studies will reveal the mechanisms underlying why GSNOR negatively regulates Cd uptake and resistance in plants, and may provide new information for the molecular breeding of non-food crops that are highly effective for the remediation of Cd-contaminated soil.

鉴于我国耕地镉污染形势严峻，以植物的镉吸收和耐性机制为理论基础，培育“镉积累量高、耐性强”的非食用性经济作物被视为一种经济高效的镉污染土壤修复途径。然而，迄今对植物应答镉胁迫机制的了解仍然有限。一氧化氮（NO）在调控植物的镉吸收和耐性中发挥重要作用。研究显示可调节胞内NO水平的S-亚硝基谷胱甘肽还原酶（GSNOR）的活性受镉胁迫显著抑制。申请人发现GSNOR功能缺失虽然增加了拟南芥的镉含量，但也增强了植物的镉耐性。基于镉胁迫-GSNOR-NO之间的潜在关联，本项目拟研究GSNOR响应镉胁迫的行为特征及其在镉引起胞内NO含量增加中的作用机制，并结合镉吸收和耐性相关基因表达及蛋白修饰的分析，从根系的镉吸收过程、细胞壁的固持镉作用、胞内的抗氧化过程等角度入手系统地研究GSNOR受抑及其引起的NO积累在增强植物的镉吸收和耐性中的分子生理机制，为培育高效修复镉污染土壤的非食用性经济作物提供理论依据。

我国耕地镉（Cd）污染问题突出，土壤Cd污染已经成为威胁我国食品安全的主要问题之一。植物应答Cd胁迫的分子生理机制，是利用生物技术或遗传育种手段培育Cd修复新品种的理论基础。本项目以拟南芥为研究材料研究了NO清除系统GSNOR在植物应答Cd胁迫过程中的作用机制。我们发现镉胁迫处理显著诱导根中GSNOR基因和GSNOR蛋白的表达，因此增强了GSNOR酶活性，而GSNOR酶活性与Cd胁迫诱导的NO积累负相关。这说明镉胁迫诱导的GSNOR活性增强有助于抑制NO的过量积累。进一步研究发现该过程通过抑制NO介导的IRT1表达，降低了根系对Cd的吸收速率，减少了根系对Cd的吸收，降低了植株的Cd含量。然而在植株地上部，Cd胁迫诱导的GSNOR酶活性增强可通过下调CAT相关基因的表达抑制CAT酶活性，进而增加植株中H2O2的积累，加剧了Cd胁迫导致氧化胁迫。本项目研究的发现有望为培育高效修复镉污染土壤的非食用性经济作物提供理论依据。