Institute of Agricultural Resources and Regional Planning, Chinese Academy of Agricultural Sciences, 12 Zhongguancun South Street, Beijing 100081, China.
Fungal Genet Biol. 2012 Jan;49(1):15-20. doi: 10.1016/j.fgb.2011.12.003. Epub 2011 Dec 17.
High temperature is one of the major impediments limiting the growth and development of most edible fungi. While many efforts have been made in agricultural practice, the mechanism for resistance to high temperature remains elusive. Nitric oxide (NO) is considered as a signaling molecule involved in regulation of diverse physiological processes and stress responses in animals and plants. However, the role of NO in regulating fungal, particularly edible fungi, response to abiotic stresses, is unknown. The present study demonstrated that NO could effectively alleviate oxidative damage induced by heat stress in mycelia of Pleurotus eryngii var. tuoliensis. Heat stress induced increased thiobarbituric acid reactive substance (TBARS) content in mycelia, and the NO donor sodium nitroprusside (SNP) dramatically decreased TBARS content under high temperature. Moreover, the specific NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-1-oxyl-3-oxide (cPTIO), could arrest the SNP action under the stress. Heat stress induced an increase in endogenous NO production in mycelial cells. However, the effect was significantly blocked by the NO synthase (NOS) inhibitor l-N(G)-nitroarginine methyl ester (l-NAME). In contrast, nitrate reductase (NR) activities were not obviously altered during heat stress. The NR suppressor tungstate had no effect on intracellular NO abundance under heat stress. These results suggest that NO can effectively protect mycelia of edible fungi from heat stress-induced oxidative damage and the NOS-dependent NO production may participate in the response to heat stress.
高温是限制大多数食用真菌生长和发育的主要障碍之一。尽管在农业实践中已经做了很多努力,但对高温抗性的机制仍然难以捉摸。一氧化氮(NO)被认为是一种信号分子,参与动物和植物中多种生理过程和应激反应的调节。然而,NO 调节真菌,特别是食用真菌,对非生物胁迫的反应的作用尚不清楚。本研究表明,NO 可以有效缓解杏鲍菇菌丝体热应激引起的氧化损伤。热应激诱导菌丝体中丙二醛(TBARS)含量增加,NO 供体硝普钠(SNP)在高温下显著降低 TBARS 含量。此外,特定的 NO 清除剂 2-(4-羧基苯基)-4,4,5,5-四甲基咪唑啉-1-1-氧化物(cPTIO)可以阻止应激下 SNP 的作用。热应激诱导菌丝细胞内内源 NO 产生增加。然而,NO 合酶(NOS)抑制剂 l-N(G)-硝基精氨酸甲酯(l-NAME)显著阻断了这一作用。相比之下,硝酸盐还原酶(NR)活性在热应激过程中没有明显改变。NR 抑制剂钨酸盐在热应激下对细胞内 NO 丰度没有影响。这些结果表明,NO 可以有效保护食用真菌的菌丝体免受热应激引起的氧化损伤,NOS 依赖性 NO 产生可能参与对热应激的反应。