MOE Key Laboratory of Environment Remediation and Ecological Health, College of Natural Resource & Environmental Sciences, Zhejiang University, Hangzhou 310058, China.
MOE Key Laboratory of Environment Remediation and Ecological Health, College of Natural Resource & Environmental Sciences, Zhejiang University, Hangzhou 310058, China.
J Hazard Mater. 2022 Oct 5;439:129600. doi: 10.1016/j.jhazmat.2022.129600. Epub 2022 Jul 14.
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 significantly decreased root activity and cell viability, and suppressed the length of root epidermal cells in the elongation 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.
在农业生态系统中释放的铟正成为一种新兴的植物胁迫源，导致细胞损伤，从而导致作物减产。以前的研究集中在铟对植物的毒性上，而植物对这种新兴金属外来化合物的适应反应却知之甚少。在这里，我们探讨了在铟胁迫下小麦根中自噬和程序性细胞死亡（PCD）的关系。铟处理显著降低了根的活性和细胞活力，并抑制了伸长区根表皮细胞的长度。这些症状可能与铟诱导的 PCD 有关，因为与未处理的根相比，铟胁迫的小麦根显示出浓缩和颗粒状的核、增加的 TUNEL 阳性核的数量、增强的核 DNA 片段化和 caspase-3 样蛋白酶活性。因此，铟增强了 TaMCA1 和 TaMCA4 的表达水平，这两个主要的介导线粒体凋亡的 metacaspase 基因在小麦植株中介导 PCD。自噬基因的增强表达和自噬体的形成表明，自噬可以调节小麦根的代谢适应和修复应激诱导的损伤。此外，通过激活剂雷帕霉素增强自噬显著降低了 TUNEL 阳性核的数量和 caspase-3 样蛋白酶的活性，而通过 3-甲基腺嘌呤抑制自噬则加剧了 PCD 的诊断标志物。这些结果共同表明，自噬抑制了小麦根中铟诱导的 PCD。
