Key Laboratory of Arid and Grassland Agroecology (Ministry of Education), School of Life Sciences, Lanzhou University, Lanzhou, 730000, People's Republic of China.
Planta. 2012 Jan;235(1):53-67. doi: 10.1007/s00425-011-1488-7. Epub 2011 Aug 4.
The roles of ethylene, hydrogen peroxide (H(2)O(2)), and calcium in inducing the capacity of the alternative respiratory pathway (AP) under chilling temperature in Arabidopsis thaliana calli were investigated. Exposure of wild-type (WT) calli, but not the calli of ethylene-insensitive mutants, etr1-3 and ein2-1, to chilling led to a marked increase of the AP capacity and triggered a rapid ethylene emission and H(2)O(2) generation. Increasing ethylene emission by applying 1-aminocyclopropane-1-carboxylic (an ethylene precursor) markedly enhanced the AP capacity in WT calli, but not in etr1-3 and ein2-1 calli, whereas suppressing ethylene emission by applying aminooxyacetic acid (an ethylene biosynthesis inhibitor) abolished the chilling-induced AP capacity in WT calli. Furthermore, exogenous H(2)O(2) treatment increased the AP capacity in WT calli, but not in etr1-3 and ein2-1 calli, while both catalase (H(2)O(2) scavenger) and diphenylene iodonium (DPI, an inhibitor of NADPH oxidase) completely inhibited the chilling-induced H(2)O(2) generation and largely inhibited the chilling-induced AP capacity. Interestingly, the chilling-induced AP capacity was completely inhibited by DPI and EGTA (calcium chelator). Further investigation demonstrated that H(2)O(2) and calcium induced ethylene emission under chilling stress. Ethylene modulated the chilling-induced increase of pyruvate content and the expression of alternative oxidase genes (AOX1a and AOX1c). Taken together, these results indicate that H(2)O(2)-, calcium- and ethylene-dependent pathways are required for chilling-induced increase in AP capacity. However, only ethylene is indispensable for the activation of the AP capacity.
研究了乙烯、过氧化氢（H2O2）和钙在诱导拟南芥愈伤组织在冷胁迫下替代呼吸途径（AP）能力中的作用。在冷胁迫下，野生型（WT）愈伤组织暴露于冷胁迫下，而乙烯不敏感突变体 etr1-3 和 ein2-1 的愈伤组织则会导致 AP 能力显著增加，并引发快速的乙烯释放和 H2O2 产生。应用 1-氨基环丙烷-1-羧酸（乙烯前体）增加乙烯的释放显著增强了 WT 愈伤组织的 AP 能力，但在 etr1-3 和 ein2-1 愈伤组织中则没有，而应用氨基氧乙酸（乙烯生物合成抑制剂）抑制乙烯的释放则消除了 WT 愈伤组织中冷胁迫诱导的 AP 能力。此外，外源性 H2O2 处理增加了 WT 愈伤组织的 AP 能力，但在 etr1-3 和 ein2-1 愈伤组织中则没有，而同时应用过氧化氢酶（H2O2 清除剂）和二苯基碘（DPI，NADPH 氧化酶抑制剂）则完全抑制了冷胁迫诱导的 H2O2 产生，并在很大程度上抑制了冷胁迫诱导的 AP 能力。有趣的是，DPI 和 EGTA（钙螯合剂）完全抑制了冷胁迫诱导的 AP 能力。进一步的研究表明，H2O2 和钙在冷胁迫下诱导乙烯的释放。乙烯调节冷胁迫诱导的丙酮酸含量增加和替代氧化酶基因（AOX1a 和 AOX1c）的表达。综上所述，这些结果表明，H2O2-、钙和乙烯依赖的途径是冷胁迫诱导 AP 能力增加所必需的。然而，只有乙烯对于激活 AP 能力是不可或缺的。
