Electron Microscopy Core Facility publications (MU)
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Items in this collection are the scholarly output of the Electron Microscopy Core Facility faculty, staff, and students, either alone or as co-authors, and which may or may not have been published in an alternate format. Items may contain more than one file type.
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Item Isolation and characterization of a baculovirus associated with the insect parasitoid wasp, Cotesia marginiventris, or its host, Trichoplusia ni(University of Wisconsin, 2008) Grasela, James J. (James John), 1951-; McIntosh, Arthur H.; Shelby, Kent S.; Long, SteveA multiple nucleopolyhedrovirus (MNPV) was isolated from Trichoplusia ni (Hübner) (Lepidoptera: Noctuidae) larvae that had been stung by the parasitoid Cotesia marginiventris (Cresson) (Hymenoptera: Braconidae). The wild type virus was plaque purified by infecting a Heliothis subflexa (BCIRL- HsAM1) cell line and isolating several clones. The mean estimated genomic size of this virus based on PstI, BstEII, StyI, HindIII restriction profiles was estimated to be 106 ± 2.5 kbp (mean±SE). A clone designated as TnMNPV/CmBCL9 was used in bioassays against several lepidopteran pests and in comparative studies with the baculoviruses AcMNPV, AgMNPV, AfMNPV, PxMNPV and HzSNPV of Autographa californica, Anticarsia gemmatalis, Anagrapha falcifera, Plutella xylostella, and Helicoverpa zea, respectively. Infectivity studies showed that TnMNPV/CmBCL9 was highly infectious for Heliothis subflexa and T. ni, with an LC50 value 0.07 occlusion bodies/mm2 in both species and also infectious for H. zea and Heliothis virescens with LC50 values of 0.22 and 0.27 occlusion bodies/mm2, respectively. Restriction endonuclease analysis of the isolate and selected baculoviruses revealed profiles that were very similar to AfMNPV but different from the restriction endonuclease profiles of the other baculoviruses. Hybridization studies suggest that the TnMNPV/CmBCL9 was closely related to AfMNPV and AcMNPV-HPP. Further support for this comes from a phylogenetic analysis employing a split-graphs network, comparing the polh, egt, and p10 genes from TnMNPV/CmBCL9 with those from other baculoviruses and suggests that this virus is closely related to the AcMNPV variants, AfMNPV and RoMNPV of Rachiplusia ou.Item Regulation of floral organ abscission in Arabidopsis thaliana(The National Academy of Sciences of the USA, 2008) Cho, Sung Ki; Larue, Clayton T., 1977-; Chevalier, David; Wang, Huachun; Jinn, Tsung-Luo; Zhang, Shuqun, 1970-; Walker, John C.; Hanʼguk Haksul Chinhŭng Chaedan; Korea Research Foundation; MU-Monsanto Graduate Research Fellowship; National Science Foundation; Food for the 21st Century (Program)Abscission is a developmental program that results in the active shedding of infected or nonfunctional organs from a plant body. Here, we establish a signaling pathway that controls abscission in Arabidopsis thaliana from ligand, to receptors, to downstream effectors. Loss of function mutations in Inflorescence Deficient in Abscission (IDA), which encodes a predicted secreted small protein, the receptor-like protein kinases HAESA (HAE) and HAESA-like 2 (HSL2), the Mitogen-Activated Protein Kinase Kinase 4 (MKK4) and MKK5, and a dominant-negative form of Mitogen-Activated Protein Kinase 6 (MPK6) in a mpk3 mutant background all have abscission-defective phenotypes. Conversely, expression of constitutively active MKKs rescues the abscission-defective phenotype of hae hsl2 and ida plants. Additionally, in hae hsl2 and ida plants, MAP kinase activity is reduced in the receptacle, the part of the stem that holds the floral organs. Plants overexpressing IDA in a hae hsl2 background have abscission defects, indicating HAE and HSL2 are epistatic to IDA. Taken together, these results suggest that the sequential action of IDA, HAE and HSL2, and a MAP kinase cascade regulates the programmed separation of cells in the abscission zone.Item Electrochemical properties of carbon nanoparticles entrapped in silica matrix(Electrochemical Society, 2008) Bok, Sangho, 1972-; Lubguban, Arnold A.; Gao, Yuanfang; Bhattacharya, Shantanu, 1974-; Korampally, Venumadhav, 1972-; Hossain, Maruf; Gangopadhyay, Shubhra; National Institutes of HealthCarbon-based electrode materials have been widely used for many years for electrochemical charge storage, energy generation, and catalysis. We have developed an electrode material with high specific capacitance by entrapping graphite nanoparticles into a sol gel network. Films from the resulting colloidal suspensions were highly porous due to the removal of the entrapped organic solvents from sol-gel matrix giving rise to high Brunauer-Emmett-Teller (BET) specific surface areas (654 m2/g)and a high capacitance density (∼37 F/g). An exponential increase of capacitance was observed with decreasing scan rates in cyclic voltammetry studies on these films suggesting the presence of pores ranging from micro (< 2 nm) to mesopores. BET surface analysis and scanning electron microscope images of these films also confirmed the presence of the micropores as well as mesopores. A steep drop in the double layer capacitance with polar electrolytes was observed when the films were rendered hydrophilic upon exposure to a mild oxygen plasma. We propose a model whereby the microporous hydrophobic sol-gel matrix perturbs the hydration of ions which moves ions closer to the graphite nanoparticles and consequently increase the capacitance of the film.Item Oxidative stress-mediated mitochondrial dysfunction contributes to angiotensin II-induced nonalcoholic fatty liver disease in transgenic ren2 rats(American Society for Investigative Pathology, 2009) Wei, Yongzhong; Clark, Suzanne E.; Thyfault, John P.; Uptergrove, Grace M.E.; Wenhan, Li; Whaley-Connell, Adam T.; Ferrario, Carlos M.; Sowers, James R. (James Russell), 1942-; Ibdah, Jamal A.; National Institutes of Health; Novartis Pharmaceutical Co.; University Of Missouri Research CouncilEmerging evidence indicates that impaired mitochondrial fatty acid [beta]-oxidation plays a key role in liver steatosis. We have recently demonstrated that increased angiotensin (ANG) II causes progressive hepatic steatosis associated with oxidative stress; however, the underlying mechanisms remain unclear. We hypothesized that ANG II causes hepatic mitochondrial oxidative damage and impairs mitochondrial [beta]-oxidation, thereby leading to hepatic steatosis. We used the Ren2 rat with elevated endogenous ANG II levels to evaluate mitochondrial ultrastructural changes, gene expression levels, and [beta]-oxidation. Compared with Sprague-Dawley littermates, Ren2 livers exhibited mitochondrial damage and reduced [beta]-oxidation, as evidenced by ultrastructural abnormalities, decrease of mitochondrial content, percentage of palmitate oxidation to CO2, enzymatic activities ([beta]-HAD and citrate synthase), and the expression levels of cytochrome c, cytochrome c oxidase subunit 1, and mitochondrial transcription factor A. These abnormalities were improved with either ANG II receptor blocker valsartan or superoxide dismutase/catalase mimetic tempol treatment. Both valsartan and tempol substantially attenuated mitochondrial lipid peroxidation in Ren2 livers. Interestingly, there was no difference in the expression of key enzymes (ACC1 and FAS) for fatty acid syntheses and their transcription factors (SREBP-1c and ChREBP) between Sprague-Dawley, untreated Ren2, and valsartan- or tempol-treated Ren2 rats. These results document that ANG II induces mitochondrial oxidative damage and impairs mitochondrial β-oxidation, contributing to liver steatosis.Item Mineralocorticoid receptor antagonism attenuates vascular apoptosis and injury via rescuing protein kinase B activation(American Heart Association, 2008) Wei, Yongzhong; Whaley-Connell, Adam T.; Habibi, Javad, 1947-; Rehmer, Jenna; Rehmer, Nathan; Patel, Kamlesh D.; Hayden, Melvin; DeMarco, Vincent G.; Ferrario, Carlos M.; Ibdah, Jamal A.; Sowers, James R. (James Russell), 1942-Emerging evidence indicates that mineralocorticoid receptor (MR) blockade reduces the risk of cardiovascular events beyond those predicted by its blood pressure-lowering actions; however, the underlying mechanisms remain unclear. To investigate whether protection elicited by MR blockade is through attenuation of vascular apoptosis and injury, independently of blood pressure lowering, we administered a low dose of the MR antagonist spironolactone or vehicle for 21 days to hypertensive transgenic Ren2 rats with elevated plasma aldosterone levels. Although Ren2 rats developed higher systolic blood pressures compared with Sprague-Dawley littermates, low-dose spironolactone treatment did not reduce systolic blood pressure compared with untreated Ren2 rats. Ren2 rats exhibited vascular injury as evidenced by increased apoptosis, hemidesmosome-like structure loss, mitochondrial abnormalities, and lipid accumulation compared with Sprague-Dawley rats, and these abnormalities were attenuated by MR antagonism. Protein kinase B activation is critical to vascular homeostasis via regulation of cell survival and expression of apoptotic genes. Protein kinase B serine473 phosphorylation was impaired in Ren2 aortas and restored with MR antagonism. In vivo MR antagonist treatment promoted antiapoptotic effects by increasing phosphorylation of BAD serine136 and expression of Bcl-2 and Bcl-xL, decreasing cytochrome c release and BAD expression, and suppressing caspase-3 activation. Furthermore, MR antagonism substantially reduced the elevated NADPH oxidase activity and lipid peroxidation, expression of angiotensin II, angiotensin type 1 receptor, and MR in Ren2 vasculature. These results demonstrate that MR antagonism protects the vasculature from aldosterone-induced vascular apoptosis and structural injury via rescuing protein kinase B activation, independent of blood pressure effects.