Plantlets of Populus yunnanensis Dode were examined in a greenhouse for 48 h to analyze their physiological and proteomic responses to sustained heat, drought, and combined heat and drought. Compared with the application of a single stress, simultaneous treatment with both stresses damaged the plantlets more heavily. The plantlets experienced two apparent response stages under sustained heat and drought. During the first stage, malondialdehyde and reactive oxygen species (ROS) contents were induced by heat, but many protective substances, including antioxidant enzymes, proline, abscisic acid (ABA), dehydrin, and small heat shock proteins (sHSPs), were also stimulated. The plants thus actively defended themselves against stress and exhibited few pathological morphological features, most likely because a new cellular homeostasis was established through the collaborative operation of physiological and proteomic responses. During the second stage, ROS homeostasis was overwhelmed by substantial ROS production and a sharp decline in antioxidant enzyme activities, while the synthesis of some protective elements, such as proline and ABA, was suppressed. As a result, photosynthetic levels in P. yunnanensis decreased sharply and buds began to die, despite continued accumulation of sHSPs and dehydrin. This study supplies important information about the effects of extreme abiotic environments on woody plants.
Both nitric oxide (NO) and hydrogen peroxide (H2 O2 ) are important signals that mediate plant response to environmental stimulation. Their role in plants' allelopathic interactions has also been reported, but the underlying mechanism remains little understood. p-Hydroxybenzoic acid (pHBA) has been proposed to be an allelopathic chemical. Here, we found that pHBA at 0.4 mM efficiently suppressed Arabidopsis growth. Meanwhile, pHBA rapidly induced the accumulation of NO and H2 O2 , where such effect could be reversed by NO or H2 O2 metabolism inhibitors or scavengers. Also, pHBA-induced NO and H2 O2 could be compromised in NO synthesis mutants noa1, nia1 and nia2, or H2 O2 metabolism mutant rbohD/F, but suppressing NO accumulation with a NO synthesis inhibitor or using NO synthesis-related mutants did not reduce pHBA-induced H2 O2 accumulation. Furthermore, we found that the effect of pHBA on allelopathic inhibition of growth was aggravated in NO/H2 O2 metabolism-related mutants or reducing NO/H2 O2 by different inhibitors, whereas the addition of an NO/H2 O2 donor could partly relieve the inhibitory effect of pHBA on the growth of wild type. However, adding only an NO donor, but not low concentration of H2 O2 as the donor, could relieve the inhibitory effect of pHBA on root growth in NO metabolism mutants. On the basis of these results, we propose that both NO and H2 O2 are important signals that mediate Arabidopsis response to the allelopathic chemical pHBA, where during this process H2 O2 may work upstream of the NO signal.
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