Light and temperature dependence of the emission of cyclic and acyclic monoterpenes from holm oak (Quercus ilex L.) leaves

In a laboratory study, we investigated the monoterpene emissions from Quercus ilex, an evergreen sclerophyllous Mediterranean oak species whose emissions are light dependent. We examined the light and temperature responses of individual monoterpenes emitted from leaves under various conditions, the effect of heat stress on emissions, and the emission-onset during leaf development. Emission rate increased 10-fold during leaf growth, with slight changes in the composition. At 30 °C and saturating light, the monoterpene emission rate from mature leaves averaged 4·1 nmol m^–2 s^–1, of which α-pinene, sabinene and β-pinene accounted for 85%. The light dependence of emission was similar for all monoterpenes: it resembled the light saturation curve of CO₂ assimilation, although monoterpene emission continued in the dark. Temperature dependence differed among emitted compounds: most of them exhibited an exponential increase up to 35 °C, a maximum at 42 °C, and a slight decline at higher temperatures. However, the two acyclic isomers cis-β-ocimene and trans-β-ocimene were hardly detected below 35 °C, but their emission rates increased above this temperature as the emission rates of other compounds fell, so that total emission of monoterpenes exponentially increased from 5 to 45 °C. The ratio between ocimene isomers and other compounds increased with both absolute temperature and time of heat exposure. The light dependence of emission was insensitive to the temperature at which it was measured, and vice versa the temperature dependence was insensitive to the light regime. The results demonstrated that none of the models currently applied to simulate isoprene or monoterpene emissions correctly predicts the short-term effects of light and temperature on Q. ilex emissions. The percentage of fixed carbon lost immediately as monoterpenes ranged between 0·1 and 6·0% depending on temperature, but rose up to 20% when leaves were continuously exposed to temperatures between 40 and 45 °C.     

南美斑潜蝇幼虫为害对黄瓜叶片中水杨酸和茉莉酸的诱导作用

【目的】为揭示南美斑潜蝇Liriomyza huidobrensis (Blanchard)与其寄主相互作用的机理, 为利用诱导抗性控制南美斑潜蝇的发生为害奠定必要的基础。【方法】本文采用高效液相色谱法（HPLC）和超高效液相色谱法-质谱联用法（UPLC MS）, 分别测定了南美斑潜蝇幼虫为害对黄瓜叶片中茉莉酸（jasmonic acid, JA）和水杨酸（salicylic acid, SA）的诱导作用。【结果】南美斑潜蝇幼虫持续为害1 d后, 受害黄瓜叶片内JA含量即显著高于健康对照, 轻度受害处理和重度受害处理分别在第3天和第5天上升幅度最大, 分别比健康对照增加2.01倍和1.62倍; 而SA含量在3 d后才显著高于健康对照, 轻度受害处理和重度受害处理在第9天上升幅度最大, 分别比健康对照增加4.66倍和1.67倍; 轻度受害对JA和SA的系统诱导作用不明显, 而重度受害对JA和SA具有明显的系统诱导作用。【结论】南美斑潜蝇幼虫为害对黄瓜叶片内JA和SA具有诱导作用。     

Expression profile of jasmonic acid-induced genes and the induced resistance against the root-knot nematode (Meloidogyne incognita) in tomato plants (Solanum lycopersicum) after foliar treatment with methyl jasmonate

We investigated what gene(s) in the plant roots have the positive role against repressing root-knot nematode (RKN) infection. We investigated the interaction between RKN infection and gene expression in the plant roots induced by methyl jasmonate (MeJA). We focused on the induced resistance response and the duration after foliar treatment with MeJA of 0.1, 0.5, 1.0, and 5.0mM at 1, 24, 48, and 72h prior to the inoculation of RKN. As a result, the foliar treatment with MeJA at 0.5mM or higher concentrations significantly reduced the infection of RKN in plants and the effect lasted for about 1 week. The repressing effect on RKN population declined to the lowest level in two weeks after MeJA treatment. The expression of proteinase inhibitors (PIs) and multicystatin (MC) were induced while the repressing effect on RKN was valid and a negative correlation was found between the expression of PIs or MC and RKN infection. In addition, when tomato plants no longer expressing MC and PIs were treated again with MeJA, the repressing effect revived. These phenomena appeared to be regardless of the existence of Mi-genes or isolate of RKN. Our results indicate that the expression level of MC and PIs may be effective as marker genes for estimating the induced resistance response against RKN infection.