10 resultados para blue-green alga

em Digital Commons at Florida International University


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Iridescent blue leaf coloration in four Malaysian rain forest understory plants, Diplazium tomentosum Bl. (Athyriaceae), Lindsaea lucida Bl. (Lindsaeaceae), Begonia pavonina Ridl. (Begoniaceae), and Phyllagathis rotundifolia Bl. (Melastomataceae) is caused by a physical effect, constructive interference of reflected blue light. The ultrastructural basis for this in D. tomentosum and L. lucida is multiple layers of cellulose microfibrils in the uppermost cell walls of the adaxial epidermis. The helicoidal arrangement of these fibrils is analogous to that which produces a similar color in arthropods. In B. pavonina and P. rotundifolia the blue-green coloration is caused by parallel lamellae in specialized plastids adjacent to the abaxial wall of the adaxial epidermis. The selective advantage of this color production, if any, is unknown.

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Iridescent blue leaf coloration in two neotropical ferns, Danaea nodosa (L.) Sm. (Marattiaceae) and Trichomanes elegans L. C. Rich. (Hymenophyllaceae), is caused by thin film constructive interference. The ultrastructural basis for the film in D. nodosa is multiple layers of cellulose microfibrils in the adaxial cell walls of the adaxial epidermis. The apparent helicoidal arrangement of the fibrils is analogous to similar color production in arthropods. In T. elegans the blue-green coloration is caused by the remarkably uniform thickness and arrangement of grana in specialized chloroplasts adjacent to the adaxial wall of the adaxial epidermis. The selective advantage of this color production, if any, is unknown but apparently different from that previously studied in Selaginella.

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Iridescent blue leaf coloration in four Malaysian rain forest understory plants, Diplazium tomentosum Bl. (Athyriaceae), Lindsaea lucida Bi. (Lindsaeaceae), Begonia pavonina Ridl. (Begoniaceae), and Phyllagathis rotundifolia Bl. (Melastoma- taceae) is caused by a physical effect, constructive interference of reflected blue light. The ultrastructural basis for this in D. tomentosum and L. lucida is multiple layers of cellulose microfibrils in the uppermost cell walls of the adaxial epidermis. The helicoidal arrangement of these fibrils is analogous to that which produces a similar color in arthropods. In B. pavonina and P. rotundifolia the blue-green coloration is caused by parallel lamellae in specialized plastids adjacent to the abaxial wall of the adaxial epidermis. The selective advantage of this color production, if any, is unknown.

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Why the leaves of many woody species accumulate anthocyanins prior to being shed has long puzzled biologists because it is unclear what effects anthocyanins may have on leaf function. Here, we provide evidence for red-osier dogwood (Cornus stolonifera) that anthocyanins form a pigment layer in the palisade mesophyll layer that decreases light capture by chloroplasts. Measurements of leaf absorbance demonstrated that red-senescing leaves absorbed more light of blue-green to orange wavelengths (495–644 nm) compared with yellow-senescing leaves. Using chlorophyll a fluorescence measurements, we observed that maximum photosystem II (PSII) photon yield of red-senescing leaves recovered from a high-light stress treatment, whereas yellow-senescing leaves failed to recover after 6 h of dark adaptation, which suggests photo-oxidative damage. Because no differences were observed in light response curves of effective PSII photon yield for red- and yellow-senescing leaves, differences between red- and yellow-senescing cannot be explained by differences in the capacities for photochemical and non-photochemical light energy dissipation. A role of anthocyanins as screening pigments was explored further by measuring the responses PSII photon yield to blue light, which is preferentially absorbed by anthocyanins, versus red light, which is poorly absorbed. We found that dark-adapted PSII photon yield of red-senescing leaves recovered rapidly following illumination with blue light. However, red light induced a similar, prolonged decrease in PSII photon yield in both red- and yellow-senescing leaves. We suggest that optical masking of chlorophyll by anthocyanins reduces risk of photo-oxidative damage to leaf cells as they senesce, which otherwise may lower the efficiency of nutrient retrieval from senescing autumn leaves.

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The increased occurrence of cyanobacteria (blue-green algae) blooms and the production of associated cyanotoxins have presented a threat to drinking water sources. Among the most common types of cyanotoxins found in potable water are microcystins (MCs), a family of cyclic heptapeptides containing substrates. MCs are strongly hepatotoxic and known to initiate tumor promoting activity. The presence of sub-lethal doses of MCs in drinking water is implicated as one of the key risk factors for an unusually high occurrence of primary liver cancer. ^ A variety of traditional water treatment methods have been attempted for the removal of cyanotoxins, but with limited success. Advanced Oxidation Technologies (AOTs) are attractive alternatives to traditional water treatments. We have demonstrated ultrasonic irradiation and UV/H2O2 lead to the degradation of cyanotoxins in drinking water. These studies demonstrate AOTs can effectively degrade MCs and their associated toxicity is dramatically reduced. We have conducted detailed studies of different degradation pathways of MCs and conclude that the hydroxyl radical is responsible for a significant fraction of the observed degradation. Results indicate preliminary products of the sonolysis of MCs are due to the hydroxyl radical attack on the benzene ring and substitution and cleavage of the diene of the Adda peptide residue. AOTs are attractive methods for treatment of cyanotoxins in potable water supplies. ^ The photochemical transformation of MCs is important in the environmental degradation of MCs. Previous studies implicated singlet oxygen as a primary oxidant in the photochemical transformation of MCs. Our results indicate that singlet oxygen predominantly leads to degradation of the phycocyanin, pigments of blue green algae, hence reducing the degradation of MCs. The predominant process involves isomerization of the diene (6E to 6Z) in the Adda side chain via photosensitized isomerization involving the photoexcited phycocyanin. Our results indicate that photosensitized processes play a key role in the environmental fate and elimination of MCs in the natural waters. ^

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Cyanobacteria (blue-green algae) produce a diverse array of toxic or otherwise bioactive metabolites. These allelochemicals may also play a role in defense against potential predators and grazers, particularly aquatic invertebrates and their larvae, including mosquitoes. Compounds derived from cyanobacteria collected from the Florida Everglades and other Florida waterways were investigated as insecticides against the mosquito Aedes aegypti, a vector of dengue and yellow fever. Screening of cyanobacterial biomass revealed several strains that exhibited mosquito larvicidal activity. Guided via bioassay guided fractionation, a non-polar compound from Leptolyngbya sp. 21-9-3 was found to be the most active component. Characterization revealed the prospective compound to be a monounsaturated fatty acid with the molecular formula C16H30O2. This is the first evidence of mosquito larvicidal activity for this particular fatty acid. With larvicidal becoming more prevalent, fatty acids should be explored for future mosquito control strategies.^

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Cyanobacteria ("blue-green algae") are known to produce a diverse repertoire of biologically active secondary metabolites. When associated with so-called "harmful algal blooms", particularly in freshwater systems, a number of these metabolites have been associated—as "toxins", or commonly "cyanotoxins"—with human and animal health concerns. In addition to the known water-soluble toxins from these genera (i.e. microcystins, cylindrospermopsin, and saxitoxins), our studies have shown that there are metabolites within the lipophilic extracts of these strains that inhibit vertebrate development in zebrafish embryos. Following these studies, the zebrafish embryo model was implemented in the bioassay-guided purification of four isolates of cyanobacterial harmful algal blooms, namely Aphanizomenon, two isolates of Cylindrospermopsis, and Microcystis, in order to identify and chemically characterize the bioactive lipophilic metabolites in these isolates. ^ We have recently isolated a group of polymethoxy-1-alkenes (PMAs), as potential toxins, based on the bioactivity observed in the zebrafish embryos. Although PMAs have been previously isolated from diverse cyanobacteria, they have not previously been associated with relevant toxicity. These compounds seem to be widespread across the different genera of cyanobacteria, and, according to our studies, suggested to be derived from the polyketide biosynthetic pathway which is a common synthetic route for cyanobacterial and other algal toxins. Thus, it can be argued that these metabolites are perhaps important contributors to the toxicity of cyanobacterial blooms. In addition to the PMAs, a set of bioactive glycosidic carotenoids were also isolated because of their inhibition of zebrafish embryonic development. These pigmented organic molecules are found in many photosynthetic organisms, including cyanobacteria, and they have been largely associated with the prevention of photooxidative damage. This is the first indication of these compounds as toxic metabolites and the hypothesized mode of action is via their biotransformation to retinoids, some of which are known to be teratogenic. Additional fractions within all four isolates have been shown to contain other uncharacterized lipophilic toxic metabolites. This apparent repertoire of lipophilic compounds may contribute to the toxicity of these cyanobacterial harmful algal blooms, which were previously attributed primarily to the presence of the known water-soluble toxins.^

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Arsenic is a ubiquitous environmental toxic substance. As a consequence of continual exposure to arsenic, nearly every organism, from Escherichia coli to humans have evolved arsenic detoxification pathways. One of the pathways is extrusion of arsenic from inside the cells, thereby conferring resistance. The R773 arsRDABC operon in E. coli encodes an ArsAB efflux pump that confers resistance to arsenite. ArsA is the catalytic subunit of the pump, while ArsB forms the oxyanion conducting pathway. ArsD is an arsenite metallochaperone that binds arsenite and transfers it to ArsA. The interaction of ArsA and ArsD allows for resistance to As(III) at environmental concentrations. The interaction between ArsA ATPase and ArsD metallochaperone was examined. A quadruple mutant in the arsD gene encoding a K2A/K37A/K62A/K104A ArsD is unable to interact with ArsA. An error-prone mutagenesis approach was used to generate random mutations in the arsA gene that restored interaction with the quadruple arsD mutant in yeast two-hybrid assays. Three such mutants encoding Q56R, F120I and D137V ArsA were able to restore interaction with the quadruple ArsD mutant. Structural models generated by in silico docking suggest that an electrostatic interface favors reversible interaction between ArsA and ArsD. Mutations in ArsA that propagate changes in hydrogen bonding and salt bridges to the ArsA-ArsD interface also affect their interactions. The second objective was to examine the mechanism of arsenite resistance through methylation and subsequent volatilization. Microbial ArsM (As(III) S-adenosylmethyltransferase) catalyzes the formation of trimethylarsine as the volatile end product. The net result is loss of arsenic from cells. The gene for CrArsM from the eukaryotic green alga Chlamydomonas reinhardtii was chemically synthesized and expressed in E. coli. The purified protein catalyzed the methylation of arsenite into methyl-, dimethyl- and trimethyl products. Synthetic purified CrArsM was crystallized in an unliganded form. Biochemical and biophysical studies conducted on CrArsM sheds new light on the pathways of biomethylation. While in microbes ArsM detoxifies arsenic, the human homolog, hAS3MT, converts inorganic arsenic into more toxic and carcinogenic forms. An understanding of the enzymatic mechanism of ArsM will be critical in deciphering its parallel roles in arsenic detoxification and carcinogenesis.

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Star formation occurs when the gas (mostly atomic hydrogen; H I) in a galaxy becomes disturbed, forming regions of high density gas, which then collapses to form stars. In dwarf galaxies it is still uncertain which processes contribute to star formation and how much they contribute to star formation. Blue compact dwarf (BCD) galaxies are low mass, low shear, gas rich galaxies that have high star formation rates when compared to other dwarf galaxies. What triggers the dense burst of star formation in BCDs but not other dwarfs is not well understood. It is often suggested that BCDs may have their starburst triggered by gravitational interactions with other galaxies, dwarf-dwarf galaxy mergers, or consumption of intergalactic gas. However, there are BCDs that appear isolated with respect to other galaxies, making an external disturbance unlikely.^ Here, I study six apparently isolated BCDs from the LITTLE THINGS sample in an attempt to understand what has triggered their burst of star formation. LITTLE THINGS is an H I survey of 41 dwarf galaxies. Each galaxy has high angular and velocity resolution H I data from the Very Large Array (VLA) telescope and ancillary stellar data. I use these data to study the detailed morphology and kinematics of each galaxy, looking for signatures of starburst triggers. In addition to the VLA data, I have collected Green Bank Telescope data for the six BCDs. These high sensitivity, low resolution data are used to search the surrounding area of each galaxy for extended emission and possible nearby companion galaxies.^ The VLA data show evidence that each BCD has likely experienced some form of external disturbance despite their apparent isolation. These external disturbances potentially seen in the sample include: ongoing/advanced dwarf-dwarf mergers, an interaction with an unknown external object, and external gas consumption. The GBT data result in no nearby, separate H I companions at the sensitivity of the data. These data therefore suggest that even though these BCDs appear isolated, they have not been evolving in isolation. It is possible that these external disturbances may have triggered the starbursts that defines them as BCDs.^

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In recent years the People’s Republic of China has begun to exhibit a more aggressive naval policy as a result of its decision to switch its naval force from a primarily green-water fleet (coastal) to a blue-water fleet (expeditionary) (“China’s New,” n.d.). This decision has brought China to loggerheads not only with other local East and South Asian powers such as India and Japan, but also with the predominant blue-water power of the world, the United States, that sees its supremacy threatened (“When Grand,” n.d.). Why would China embark on a route that would pit it against the world naval superpower, the United States, which has a huge lead on China in terms of naval blue-water power? Why would China try to challenge and match the U.S. Navy’s eleven aircraft carriers (“The World’s,” n.d.)? What could compel China to embark on a plan that would so disrupt the balance of power in the waters around Asia? To fully understand the Chinese government’s decision, one must first look at Chinese import figures and Chinese trade routes.