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The rhizostome jellyfish Nemopilema nomurai, which is endemic to the East Asian Marginal Seas (i.e. the Bohai, Yellow, East China and Japan Seas), is unique both by its enormous body size (ca. 2 m maximum bell diameter and 200 kg wet weight) and propensity for occasional population explosions. Massive blooms of this species have historically been reported only once per ca. 40 years (i.e. in 1920, 1958 and 1995), but have become increasingly frequent recently (i.e. in 2002, 2003, 2005 and 2006). Both accumulated knowledge on the spatiotemporal distributions and physical modeling of the water circulation show that the medusae are released from benthic polyps during April-June in the Yellow Sea and East China Sea, and transported by the Tsushima Current to the Japan Sea. The bloom in 2005 might be the largest ever in history; as many as 3-5 x l0E8 medusae passed through the Tsushima Strait daily during the summer and there were more than 100,000 complaints from commercial fishermen. The recent blooms of N. nomurai may have been caused by environmental changes, such as increased water temperature, eutrophication, coastal modification, and over-fishing in Chinese coastal waters. Frequent jellyfish blooms can apparently be a threat to the fisheries sustainability of the East Asian Marginal Seas, one of the world's most productive fisheries grounds.

Plants respond to physical injury, such as that caused by foraging insects, by synthesizing proteins that function in general defense and tissue repair. In tomato plants, one class of wound-responsive genes encodes proteinase inhibitor (pin) proteins shown to block insect feeding. Application of many different factors will induce or inhibit pin gene expression. Ethylene is required in the transduction pathway leading from injury, and ethylene and jasmonates act together to regulate pin gene expression during the wound response

We investigated how salicylic acid (SA) enhances H2O2 and the relative significance of SA-enhanced H2O2 in Arabidopsis thaliana. SA treatments enhanced H2O2 production, lipid peroxidation, and oxidative damage to proteins, and resulted in the formation of chlorophyll and carotene isomers. SA-enhanced H2O2 levels were related to increased activities of Cu,Zn-superoxide dismutase and were independent of changes in catalase and ascorbate peroxidase activities. Prolonging SA treatments inactivated catalase and ascorbate peroxidase and resulted in phytotoxic symptoms, suggesting that inactivation of H2O2-degrading enzymes serves as an indicator of hypersensitive cell death. Treatment of leaves with H2O2 alone failed to invoke SA-mediated events. Although leaves treated with H2O2 accumulated in vivo H2O2 by 2-fold compared with leaves treated with SA, the damage to membranes and proteins was significantly less, indicating that SA can cause greater damage than H2O2. However, pretreatment of leaves with dimethylthiourea, a trap for H2O2, reduced SA-induced lipid peroxidation, indicating that SA requires H2O2 to initiate oxidative damage. The relative significance of the interaction among SA, H2O2 and H2O2-metabolizing enzymes with oxidative damage and cell death is discussed

Aluminum (Al) is the most abundant metal in the earth's crust, comprising about 7% of its mass. Since many plant species are sensitive to micromolar concentrations of Al, the potential for soils to be Al toxic is considerable. Fortunately, most of the Al is bound by ligands or occurs in other nonphytotoxic forms such as aluminosilicates and precipitates. However, solubilization of this Al is enhanced by low pH and Al toxicity is a major factor limiting plant production on acid soils. Soil acidification can develop naturally when basic cations are leached from soils, but it can be accelerated by some farming practices and by acid rain (Kennedy, 1986). Strategies to maintain production on these soils include the application of lime to raise the soil pH and the use of plants that are tolerant of acid soils. Although Al toxicity has been identified as a problem of acid soils for over 70 years, our knowledge about the primary sites of toxicity and the chain of events that finally affects plant growth remains largely speculative. In this paper we review recent progress that has been made in our understanding of Al toxicity and the mechanisms of Al tolerance in plants

The application of a moderate water deficit (water potential of -1.3 MPa) to pea (Pisum sativum L. cv Lincoln) leaves led to a 75% inhibition of photosynthesis and to increases in zeaxanthin, malondialdehyde, oxidized proteins, and mitochondrial, cytosolic, and chloroplastic superoxide dismutase activities. Severe water deficit (-1.9 MPa) almost completely inhibited photosynthesis, decreased chlorophylls, beta-carotene, neoxanthin, and lutein, and caused further conversion of violaxanthin to zeaxanthin, suggesting damage to the photosynthetic apparatus. There were consistent decreases in antioxidants and pyridine nucleotides, and accumulation of catalytic Fe, malondialdehyde, and oxidized proteins. Paraquat (PQ) treatment led to similar major decreases in photosynthesis, water content, proteins, and most antioxidants, and induced the accumulation of zeaxanthin and damaged proteins. PQ decreased markedly ascorbate, NADPH, ascorbate peroxidase, and chloroplastic Fe-superoxide dismutase activity, and caused major increases in oxidized glutathione, NAD+, NADH, and catalytic Fe. It is concluded that, in cv Lincoln, the increase in catalytic Fe and the lowering of antioxidant protection may be involved in the oxidative damage caused by severe water deficit and PQ, but not necessarily in the incipient stress induced by moderate water deficit. Results also indicate that the tolerance to water deficit in terms of oxidative damage largely depends on the legume cultivar

Hydroxyl radicals may be responsible for oxidative damage during drought or chilling stress. We have shown that the presence of mannitol in chloroplasts can protect plants against oxidative damage by hydroxyl radicals (B. Shen, R.G. Jensen, H.J. Bohnert [1997] Plant Physiol 113:1177-1183). Here we identify one of the target enzymes that may be protected by mannitol. Isolated thylakoids in the presence of physiological concentrations of Fe2+ generated hydroxyl radicals that were detected by the conversion of phenylalanine into tyrosine. The activity of phosphoribulokinase (PRK), a thiol-regulated enzyme of the Calvin cycle, was reduced by 65% in illuminated thylakoids producing hydroxyl radicals. Mannitol (125 mM) and sodium formate (15 mM), both hydroxyl radical scavengers, and catalase (3000 units mL-1) prevented loss of PRK activity. In contrast, superoxide dismutase (300 units mL-1) and glycine betaine (125 mM) were not effective in protecting PRK against oxidative inactivation. Ribulose-1,5-bisphosphate carboxylase/oxygenase activity was not affected by hydroxyl radicals. We suggest that the stress-protective role of mannitol may be to shield susceptible thiol-regulated enzymes like PRK plus thioredoxin, ferredoxin, and glutathione from inactivation by hydroxyl radicals in plants

We have assessed ultraviolet-B (UV-B)-induced injury in wild-type Arabidopsis thaliana and two mutants with altered aromatic secondary product biosynthesis. Arabidopsis mutants defective in the ability to synthesize UV-B-absorbing compounds (flavonoids in transparent testa 5 [tt5] and sinapate esters in ferulic acid hydroxylase 1 [fah1]) are more sensitive to UV-B than is the wild-type Landsberg erecta. Despite its ability to accumulate UV-absorptive flavonoid compounds, the ferulic acid hydroxylase mutant fah1 exhibits more physiological injury (growth inhibition and foliar lesions) than either wild type or tt5. The extreme UV-B sensitivity of fah1 demonstrates the importance of hydroxycinnamate esters as UV-B protectants. Consistent with the whole-plant response, the highest levels of lipid and protein oxidation products were seen in fah1. Ascorbate peroxidase enzyme activity was also increased in the leaves of UV-B-treated plants in a dose- and genotype-dependent manner. These results demonstrate that, in A. thaliana, hydroxycinnamates are more effective UV-B protectants than flavonoids. The data also indicate that A. thaliana responds to UV-B as an oxidative stress, and sunscreen compounds reduce the oxidative damage caused by UV-B

We investigated the relationship between the expression of lipoxygenase (LOX) genes and the systemin-dependent wound response in tomato (Lycopersicon esculentum) leaves. A polymerase chain reaction-based approach was used to isolate two tomato Lox cDNAs, called TomLoxC and TomLoxD. Both TomLOXC and TomLOXD amino acid sequences possess an N-terminal extension of about 60 residues that were shown by in vitro uptake to function as transit peptides, targeting these proteins into the chloroplast. Within 30 to 50 min following wounding or systemin or methyl jasmonate treatments, the TomLoxD mRNA level increased and reached a maximum between 1 and 2 h. TomLoxC mRNA was not detectable in leaves and was not found following wounding, but it was found in ripening fruits, indicating that the two tomato Lox genes are regulated in different tissues by different processes. The results suggest that the TomLoxD gene is up-regulated in leaves in response to wounding and encodes a chloroplast LOX that may play a role as a component of the octadecanoid defense-signaling pathway

The timing of transcript accumulation of several wound-induced genes is different in insect-damaged and mechanically damaged leaves. Transcripts for the proteinase inhibitor II and 3-hydroxy-3-methylglutaryl-coenzyme A reductase genes accumulate more rapidly in potato (Solanum tuberosum L.) leaves chewed on by caterpillars than in leaves damaged mechanically. The timing of maximum transcript accumulation was not affected by the degree of damage inflicted by the insect larvae. When applied to a mechanical wound site, regurgitant isolated from Manduca sexta larvae causes transcript accumulation profiles to shift to parallel those in insect-damaged tissue. Whether obtained from larvae fed either potato leaves or a nonplant diet, insect regurgitant fed through the petiole of detached leaves also induces accumulation of these transcripts. The transcript accumulation-inducing activity of regurgitant is enhanced by heating at 100 degrees C. Our data suggest that a heat-stable, insect-derived elicitor functions to induce the rapid accumulation of transcripts that may be involved in plant defense against herbivores. Distinct signal transduction pathways that can distinguish between insect damage and abiotic damage might therefore exist in plants

An intracellular signaling pathway for activating plant defense genes against attacking herbivores and pathogens is mediated by a lipid-based signal transduction cascade. In this pathway, linolenic acid (18:3) is proposed to be liberated from cell membranes and is converted to cyclopentanones that are involved in transcriptional regulation of defense genes, analogously to prostaglandin synthesis and function in animals. Levels of 18:3 and linoleic acid in tomato (Lycopersicon esculentum) leaves increased within 1 h when the leaves were wounded with a hemostat across the main vein to simulate herbivore attacks. The increase correlated with the time course of accumulation of jasmonic acid, a cyclopentanone product of 18:3, that had previously been shown to increase in leaves in response both to wounding and to elicitors of plant defense genes. One hour after wounding, at least a 15-fold excess of 18:3 was found over that required to account for the levels of newly synthesized jasmonic acid. The free fatty acids in both control and wounded leaves accounted for less than 0.25% of the total fatty acids. However, the total lipid contents of the leaves remained relatively unchanged up to 8 h after wounding, indicating that extensive loss of lipids did not occur, although a gradual decrease in polar lipids was observed, mainly in monogalactosyl diacylglycerol of chloroplast lipids. The data support a role for lipid release as a key step in the signaling events that activate defense genes in tomato leaves in response to wounding by attacking herbivores