Lawrence Berkeley National Lab, Climate and Ecosystem Science Division, Berkeley, California, USA.
Environmental Molecular Sciences Laboratory, Pacific Northwest National Lab, Richland, Washington, USA.
Plant Cell Environ. 2022 Dec;45(12):3429-3444. doi: 10.1111/pce.14464. Epub 2022 Oct 20.
Growth suppression and defence signalling are simultaneous strategies that plants invoke to respond to abiotic stress. Here, we show that the drought stress response of poplar trees (Populus trichocarpa) is initiated by a suppression in cell wall derived methanol (MeOH) emissions and activation of acetic acid (AA) fermentation defences. Temperature sensitive emissions dominated by MeOH (AA/MeOH <30%) were observed from physiologically active leaves, branches, detached stems, leaf cell wall isolations and whole ecosystems. In contrast, drought treatment resulted in a suppression of MeOH emissions and strong enhancement in AA emissions together with volatiles acetaldehyde, ethanol, and acetone. These drought-induced changes coincided with a reduction in stomatal conductance, photosynthesis, transpiration, and leaf water potential. The strong enhancement in AA/MeOH emission ratios during drought (400%-3500%) was associated with an increase in acetate content of whole leaf cell walls, which became significantly C -labelled following the delivery of C -acetate via the transpiration stream. The results are consistent with both enzymatic and nonenzymatic MeOH and AA production at high temperature in hydrated tissues associated with accelerated primary cell wall growth processes, which are downregulated during drought. While the metabolic source(s) require further investigation, the observations are consistent with drought-induced activation of aerobic fermentation driving high rates of foliar AA emissions and enhancements in leaf cell wall O-acetylation. We suggest that atmospheric AA/MeOH emission ratios could be useful as a highly sensitive signal in studies investigating environmental and biological factors influencing growth-defence trade-offs in plants and ecosystems.
生长抑制和防御信号是植物应对非生物胁迫的同时策略。在这里，我们表明，杨树（Populus trichocarpa）对干旱胁迫的反应是由细胞壁衍生甲醇（MeOH）排放的抑制和乙酸（AA）发酵防御的激活引发的。从生理活跃的叶片、枝条、离体茎、叶细胞壁分离和整个生态系统中观察到以 MeOH 为主的温度敏感排放（AA/MeOH<30%）。相比之下，干旱处理导致 MeOH 排放的抑制和 AA 排放的强烈增强，以及挥发性乙醛、乙醇和丙酮。这些干旱诱导的变化与气孔导度、光合作用、蒸腾和叶片水势的降低同时发生。干旱期间 AA/MeOH 排放比值的强烈增强（400%-3500%）与整个叶细胞壁中乙酸含量的增加有关，在用蒸腾流输送 13C-乙酸后，细胞壁的乙酸含量显著增加。结果与高温下含水组织中酶促和非酶促 MeOH 和 AA 产生一致，与加速初生细胞壁生长过程有关，而在干旱期间，这些过程被下调。虽然代谢源需要进一步研究，但这些观察结果与干旱诱导的有氧发酵激活一致，该发酵驱动叶片 AA 排放的高速率和叶细胞壁 O-乙酰化的增强。我们认为，大气 AA/MeOH 排放比值可以作为研究影响植物和生态系统生长-防御权衡的环境和生物因素的高度敏感信号。
