Regulation of Tolerance of Chlamydomonas reinhardtii to Heavy Metal Toxicity by Heme Oxygenase-1 and Carbon Monoxide

被引:51
作者
Wei, Yuan Yuan [1 ,2 ]
Zheng, Qi [1 ]
Liu, Zhao Pu [2 ]
Yang, Zhi Min [1 ]
机构
[1] Nanjing Agr Univ, Dept Biochem & Mol Biol, Coll Life Sci, Nanjing 210095, Peoples R China
[2] Nanjing Agr Univ, Key Lab Marine Biol Jiang Su, Nanjing 210095, Peoples R China
基金
中国国家自然科学基金;
关键词
Chlamydomonas reinhardtii; Heavy metal; Heme oxygenase; INDUCED OXIDATIVE STRESS; NITRIC-OXIDE; MERCURY TOXICITY; UP-REGULATION; CELL-DEATH; EXPRESSION; GENE; BIOACCUMULATION; FLUORESCENCE; ARABIDOPSIS;
D O I
10.1093/pcp/pcr102
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Investigation of heavy metal tolerance genes in green algae is of great importance because heavy metals have become one of the major contaminants in the aquatic ecosystem. In plants, accumulation of heavy metals modifies many aspects of cellular functions. However, the mechanism by which heavy metals exert detrimental effects is poorly understood. In this study, we identified a role for HO-1 (encoding heme oxygenase-1) in regulating the response of Chlamydomonas reinhardtii, a unicellular green alga, to mercury (Hg). Transgenic algae overexpressing HO-1 showed high tolerance to Hg exposure, with a 48.2% increase in cell number over the wild type, but accumulated less Hg. Physiological analysis revealed that expression of HO-1 suppressed the Hg-induced generation of reactive oxygen species. We further identified the effect of carbon monoxide (CO), a product of HO-1-mediated heme degradation, on growth and physiological parameters. Interestingly, administration of exogenous CO at non-toxic levels also conferred the tolerance of algae to Hg exposure. The CO-mediated alleviation of Hg toxicity was closely related to the lower accumulation of Hg and free radical species. These results indicate that functional identification of HO-1 is useful for molecular breeding designed to improve plant tolerance to heavy metals and reduce heavy metal accumulation in plant cells.
引用
收藏
页码:1665 / 1675
页数:11
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