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Stomatal opening provides access to inner leaf tissues for many plant pathogens, so narrowing stomatal apertures may be advantageous for plant defense. We investigated how guard cells respond to elicitors that can be generated from cell walls of plants or pathogens during pathogen infection. The effect of oligogalacturonic acid (OGA), a degradation product of the plant cell wall, and chitosan (beta-1,4-linked glucosamine), a component of the fungal cell wall, on stomatal movements were examined in leaf epidermis of tomato (Lycopersicon esculentum L.) and Commelina communis L. These elicitors reduced the size of the stomatal aperture. OGA not only inhibited light-induced stomatal opening, but also accelerated stomatal closing in both species; chitosan inhibited light-induced stomatal opening in tomato epidermis. The effects of OGA and chitosan were suppressed when EGTA, catalase, or ascorbic acid was present in the medium, suggesting that Ca(2+) and H(2)O(2) mediate the elicitor-induced decrease of stomatal apertures. We show that the H(2)O(2) that is involved in this process is produced by guard cells in response to elicitors. Our results suggest that guard cells infected by pathogens may close their stomata via a pathway involving H(2)O(2) production, thus interfering with the continuous invasion of pathogens through the stomatal pores.  相似文献   
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Chloroplast DNA (cpDNA) is most often maternally inherited and highly conserved leading to previous observation of little to no sequence variation. Comparing cpDNA haplotypes have provided valuable insight into the establishment and migration of polyploid populations. However, to use chloroplast haplotypes to their full potential intrapopulational variation needs to be addressed. In this study, cpDNA haplotype variation was surveyed within 16 natural populations of prairie cordgrass (Spartina pectinata Link) located east of the 100th west meridian and north of the 35th north parallel in the U.S.A. using two non-coding, polymorphic chloroplast regions. Two main clades were defined with subclades as follows: haplotype 1 and haplotype 2A and 2B. It was discovered that seven populations showed intrapopulational chloroplast genome variation. Of the total amount of variation, 95.5% occurred within the octoploid populations and 4.5% occurred within the tetraploid populations. Both variant haplotypes, 2A and 2B, were found in a larger sampling of one of the natural populations, but no variation was found in a mixed ploidy population. The intrapopulational cpDNA variation we found in this study cannot directly be related to mechanisms of introduction of the non-native populations into native populations. Therefore, this cpDNA variation could be novel natural variation that has been fixed as the octoploid populations were established and moved northwest. This analysis provides insight into determining the usefulness of indels and single nucleotide polymorphisms for population identification and may provide information in regards to the origin of chloroplast variation and its subsequent fixation and establishment in natural prairie cordgrass populations.  相似文献   
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Conotoxins are well known for their highly variable structures and functions. Here we report the identification of a novel conotoxin named mr1e from Conus marmoreus . mr1e is composed of 11 amino acid residues cross-linked by two disulfide bonds (CCHSSWCKHLC). The spacing of intercysteine loops in mr1e is exactly the same as that in α4/3 conotoxins. However, the native mr1e peptide co-eluted on reverse-phase HPLC with the regioselectively synthesized ribbon disulfide linkage isomer (C1-C4, C2-C3) but not the globular linkage isomer (C1-C3, C2-C4). Although this peptide has the same disulfide connectivity as the χ-conotoxins, their sequences do not share significant homology. Thus, mr1e could be defined as a novel conotoxin family. By intracranial injection into mice, mr1e showed an excitatory effect. The characterization of mr1e certainly enriches our understanding of conotoxins, and also opens an avenue for further structural and functional investigation.  相似文献   
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Phosphatidic acid activates a wound-activated MAPK in Glycine max   总被引:3,自引:0,他引:3  
Many plant species demonstrate a systemic increase in phosphatidic acid (PA) levels after being wounded (Lee et al., 1997). To understand the role of PA in wound signal transduction, we investigated if PA can activate protein kinases in soybean (Glycine max L.). We found that a MAPK is activated in soybean seedlings in both wounded and neighboring unwounded leaves. The wound-activated soybean kinase is specifically recognized by an antibody against the alfalfa MAPK, SIMK. When PA production is inhibited with n-butanol, an inhibitor of phospholipase D, the wound-induced activation of the MAPK is suppressed, suggesting that an elevation in PA levels is essential for its activation. Supporting this is the observation that exogenous PA activates the MAPK in suspension-cultured soybean cells. Activation of the 49 kDa MAPK occurs almost exclusively by PA, as other lipids are unable to or can only weakly activate the kinase. PA-induced activation of the MAPK is not a direct effect on the kinase but is mediated by upstream kinases. Our results suggest that PA acts as a second messenger in wound-induced MAPK signaling in plants.  相似文献   
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Taihu Lake is one of the largest freshwater lakes in China. The lake is very shallow with a mean depth of 1.9 m and an area of 2428 km2. This is the first time that polycyclic aromatic hydrocarbon concentrations in the surface sediments of Taihu Lake have been analyzed. A distinctive spatial distribution of PAHs was observed. Sediments from Lake Wulihu and Meiliang Bay (sites 1–5) had significantly higher PAH concentrations (858–5260 g kg–1 dw) than any other area of Taihu Lake. These high PAH levels were associated with the input of untreated and partially treated domestic and industrial sewage from Wuxi, Changzhou, Wujin and other cities. Special PAH ratios, such as phenanthrene/anthracene and fluoranthene/pyrene, were calculated to evaluate the relative importance of different origins. The data confirmed a relatively high level of petrogenic contamination in sites 1–5 (mainly sewage discharge and the river runoff). The other samples were further from the sources of pollution and have relatively low PAH concentrations (410–768 g kg–1 dw). The sources of PAHs in these sites (6–13) were characterized by combustion-derived PAH contamination associated with atmospheric deposition. In addition, effects range low (ERL) and effects range median (ERM) guidelines (Long et al., 1995) were used to estimate the potential of adverse effects resulting from PAH contamination in Taihu Lake sediments. The results indicated that some sites in the northern part of the lake had levels of PAH that exceeded the ERL value. This was interpreted to mean that acute biological effects may occasionally be expected to occur.  相似文献   
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Inhibition of high mobility group box 1 (HMGB1) and restoration of endothelial integrity are emerging as attractive therapeutic strategies for the management of severe vascular inflammatory diseases. Recently, we found that JH-4, a synthesized decursin derivative, exhibited a strong anti-Hutchinson-Gilford progeria syndrome by efficiently blocking progerin-lamin A/C binding. In this study, we examined the effects of JH-4 on HMGB1-mediated septic responses and the survival rate in a mouse sepsis model. The anti-inflammatory activities of JH-4 were monitored based on its effects on lipopolysaccharide- or cecal ligation and puncture (CLP)-mediated release of HMGB1. The antiseptic activities of JH-4 were determined by measuring permeability, leukocyte adhesion, migration, and the activation of proinflammatory proteins in HMGB1-activated human umbilical vein endothelial cells and mice. JH-4 inhibited the release of HMGB1 and downregulated HMGB1-dependent inflammatory responses in human endothelial cells. JH-4 also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice. In addition, treatment with JH-4 reduced CLP-induced release of HMGB1, sepsis-related mortality, and pulmonary injury in vivo. Our results indicate that JH-4 is a possible therapeutic agent to treat various severe vascular inflammatory diseases via the inhibition of the HMGB1 signaling pathway.  相似文献   
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