Physiological and protein responses in leaves of Nitraria billardieri seedlings to moderate salt stress

被引:2
|
作者
Tian, Lin [1 ,3 ]
Zhu, Liming [2 ]
Cheng, Tielong [2 ]
Xia, Xinli [1 ]
Yin, Weilun [1 ]
机构
[1] Beijing Forestry Univ, Coll Biol Sci & Biotechnol, Beijing Adv Innovat Ctr Tree Breeding Mol Design, Natl Engn Lab Tree Breeding, Beijing, Peoples R China
[2] Nanjing Forestry Univ, Dept Ecol, Coll Biol & Environm, Nanjing, Jiangsu, Peoples R China
[3] Chinese Acad Forestry, State Key Lab Tree Genet & Breeding, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
Nitraria billardieri; salt stress; physiological response; proteomic profiling; metabolic pathways; MAIZE INBRED LINES; THELLUNGIELLA-HALOPHILA; PROTEOMIC ANALYSIS; ARABIDOPSIS-THALIANA; SALINITY TOLERANCE; MECHANISMS; DROUGHT; PROLINE; ACCUMULATION; SELECTIVITY;
D O I
10.1080/17429145.2018.1526979
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Salt stress is a major environmental factor affecting plant growth and geographical distribution. Halophytes are considered valuable resources for investigating plant tolerance mechanisms. The halophyte Nitraria billardieri is widely distributed in saline soil in Australia and China. To investigate salt stress-induced changes at the physiological and molecular levels in N.billardieri, three-month-old seedlings were subjected to salt stress treatments. The physiological and biochemical analyses showed that N.billardieri seedlings could adapt to and strongly tolerate salt stress by accumulating soluble sugars and proline as organic osmolytes and increasing the activities of antioxidative enzymes. Comparative proteomic and metabolic pathway analyses revealed 130 differentially expressed proteins, which displayed various response patterns under salt stress. A protein interaction analysis found that the interaction consisting of amino acid and carbohydrate metabolism coupled with redox homeostasis and protein synthesis may play an essential role in response to salt stress in N.billardieri seedlings. Overall, salt stress treatment disrupted a cascade of normal metabolic programing and subsequently caused oxidative and osmotic stress by altering protein fates, signal transduction and redox homeostasis.
引用
收藏
页码:522 / 531
页数:10
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