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乙烯通过清除蚕豆保卫细胞中的一氧化氮来抑制黑暗诱导的气孔关闭。

Ethylene inhibits darkness-induced stomatal closure by scavenging nitric oxide in guard cells of Vicia faba.

作者信息

Song Xi-Gui, She Xiao-Ping, Wang Juan, Sun Yi-Chao

机构信息

School of Life Sciences, Shaanxi Normal University, Xi'an 710062, People's Republic of China.

出版信息

Funct Plant Biol. 2011 Oct;38(10):767-777. doi: 10.1071/FP11055.

DOI:10.1071/FP11055
PMID:32480934
Abstract

The plant hormone ethylene regulates many aspects of plant growth and development. Despite the well-known relationship between ethylene and stress signalling, the involvement of ethylene in regulating stomatal movement is not completely explored. Here, the role and association between nitric oxide (NO) reduction and the inhibition of darkness-induced stomatal closure by ethylene was studied. Physiological data are provided that both ethylene-releasing compound 2-chloroethylene phosphonic acid (ethephon, ETH) and 1-aminocyclopropane-1-carboxylic acid (ACC), the immediate precursor of ethylene, reduced the levels of NO in Vicia faba L. guard cells, and then induced stomatal opening in darkness. In addition, ACC and ETH not only reduced NO levels in guard cells caused by exogenous NO (derived from sodium nitroprusside, SNP) in light, but also abolished NO that had been generated during a dark period and promoted stomatal opening. Interestingly, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) and hemoglobin (Hb), NO scavenger and the potent scavenger of NO/carbon monoxide (CO), respectively, also reduced NO levels by SNP and darkness. However, the above-mentioned effects of ACC and ETH were dissimilar to that of nitric oxide synthase (enzyme commission 1.14.13.39) inhibitor NG-nitro-L-Arg-methyl ester (L-NAME), which could neither reduce NO levels by SNP nor abolish NO that had been generated in the dark. Thus, it is concluded that ethylene reduces the levels of NO in V. faba guard cells via a pattern of NO scavenging, then induces stomatal opening in the dark.

摘要

植物激素乙烯调节植物生长和发育的许多方面。尽管乙烯与胁迫信号传导之间的关系广为人知,但乙烯在调节气孔运动中的作用尚未得到充分研究。在此,研究了一氧化氮(NO)还原与乙烯抑制黑暗诱导的气孔关闭之间的作用及关联。提供的生理数据表明,乙烯释放化合物2-氯乙基膦酸(乙烯利,ETH)和乙烯的直接前体1-氨基环丙烷-1-羧酸(ACC)均降低了蚕豆保卫细胞中的NO水平,进而诱导黑暗中的气孔开放。此外,ACC和ETH不仅降低了光照下外源NO(源自硝普钠,SNP)引起的保卫细胞中的NO水平,还消除了在黑暗期产生的NO并促进了气孔开放。有趣的是,2-(4-羧基苯基)-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物(cPTIO)和血红蛋白(Hb),分别为NO清除剂和NO/一氧化碳(CO)的有效清除剂,也通过SNP和黑暗降低了NO水平。然而,ACC和ETH的上述作用与一氧化氮合酶(酶委员会编号为)抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)不同,L-NAME既不能通过SNP降低NO水平,也不能消除在黑暗中产生的NO。因此,得出的结论是,乙烯通过清除NO的方式降低蚕豆保卫细胞中的NO水平,进而诱导黑暗中的气孔开放。

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Ethylene inhibits darkness-induced stomatal closure by scavenging nitric oxide in guard cells of Vicia faba.乙烯通过清除蚕豆保卫细胞中的一氧化氮来抑制黑暗诱导的气孔关闭。
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