Autophagy alleviates indium-induced programmed cell death in wheat roots

被引:12
|
作者
Qian, Ruyi [1 ]
Zhao, Hongcheng [1 ]
Liang, Xin [1 ]
Sun, Nan [1 ]
Zhang, Nan [1 ]
Lin, Xianyong [1 ]
Sun, Chengliang [1 ]
机构
[1] Zhejiang Univ, Coll Nat Resource & Environm Sci, MOE Key Lab Environm Remediat & Ecol Hlth, Hangzhou 310058, Peoples R China
基金
中国国家自然科学基金;
关键词
Indium; Programmed cell death; Autophagy; Wheat; Stress; DNA-DAMAGE; STRESS; OXIDE; TOLERANCE; TOXICITY; LIFE;
D O I
10.1016/j.jhazmat.2022.129600
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Indium released in agroecosystems is becoming an emerging plant stressor, causing cellular damage and consequently crop yield losses. Previous studies have focused on indium-induced toxicity in plants, while plant adaptive responses to such emerging metal xenobiotics are poorly understood. Here, we explored the relationship of autophagy and programmed cell death (PCD) in wheat roots under indium stress. Indium treatment signifi-cantly decreased root activity and cell viability, and suppressed the length of root epidermal cells in the elon-gation zones. These symptoms may be associated with indium-induced PCD, as indium-stressed wheat roots displayed condensed and granular nuclei, increased number of TUNEL-positive nuclei, enhanced nuclear DNA fragmentation and caspase-3-like protease activity compared to untreated roots. Accordingly, indium enhanced the expression levels of TaMCA1 and TaMCA4, two major metacaspase genes mediated PCD in wheat plants. The enhanced expression of autophagy genes and formation of autophagosomes indicate that autophagy could regulate metabolic adaptation and repair stress-induced damage in wheat roots. Furthermore, reinforcing autophagy by activator rapamycin significantly decreased the number of TUNEL-positive nuclei and the activity of caspase-3-like protease, whereas inhibition of autophagy by 3-methyladenine aggravated diagnostic markers for PCD. These results together suggest that autophagy suppresses indium-induced PCD in wheat roots.
引用
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页数:10
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