Relevant bibliographies by topics / Cell biology, n.e.c

Academic literature on the topic 'Cell biology, n.e.c'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Cell biology, n.e.c"

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Van Langevelde, Arjen, Kees Van Malssen, René Driessen, Kees Goubitz, Frank Hollander, René Peschar, Peter Zwart, and Henk Schenk. "Structure of C n C n+2C n -type (n = even) β′-triacylglycerols." Acta Crystallographica Section B Structural Science 56, no. 6 (December 1, 2000): 1103–11. http://dx.doi.org/10.1107/s0108768100009927.

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The crystal structures of the β′ phase of CLC (1,3-didecanoyl-2-dodecanoylglycerol) and MPM (1,3-ditetradecanoyl-2-hexadecanoylglycerol) have been determined from single-crystal X-ray diffraction and high-resolution X-ray powder diffraction data, respectively. Both these crystals are orthorhombic with space group Iba2 and Z = 8. The unit-cell parameters of β′-CLC are a = 57.368 (6), b = 22.783 (2) and c = 5.6945 (6) Å and the final R value is 0.175. The unit-cell parameters of β′-MPM are a = 76.21 (4), b = 22.63 (1) and c = 5.673 (2) Å and the final Rp value is 0.057. Both the β′-CLC and β′-MPM molecules are crystallized in a chair conformation, having a bend at the glycerol moiety. The zigzag planes of the acyl chains are orthogonally packed, as is typical for a β′ phase. Furthermore, unit-cell parameters of some other members of the C n C n+2C n -type triacylglycerol series have been refined on their high-resolution X-ray powder diffraction pattern. Finally, the crystal structures are compared with the currently known structures and models of triacylglycerols.
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Leibovitch, Marie-Pierre, Serge A. Leibovitch, Josette Hillion, Martine Guillier, Annette Schmitz, and Jacques Harel. "Possible role of c-fos, c-N-ras and c-mos proto-oncogenes in muscular development." Experimental Cell Research 170, no. 1 (May 1987): 80–92. http://dx.doi.org/10.1016/0014-4827(87)90118-2.

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Miñana, MaDolores, Vicente Felipo, and Santiago Grisolía. "Differential effects of the protein kinase C inhibitors H7 and calphostin C on the cell cycle of neuroblastoma cells." Brain Research 596, no. 1-2 (November 1992): 157–62. http://dx.doi.org/10.1016/0006-8993(92)91543-n.

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Yang, Ruojing, and James M. Trevillyan. "c-Jun N-terminal kinase pathways in diabetes." International Journal of Biochemistry & Cell Biology 40, no. 12 (January 2008): 2702–6. http://dx.doi.org/10.1016/j.biocel.2008.06.012.

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Krapp, Anne, Vera Saliba-Colombani, and Françoise Daniel-Vedele. "Analysis of C and N metabolisms and of C/N interactions using quantitative genetics." Photosynthesis Research 83, no. 2 (February 2005): 251–63. http://dx.doi.org/10.1007/s11120-004-3196-7.

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FORMICKA-KOZLOWSKA, Grazyna, Helga SCHNEIDER-BERNLOHR, Jean-Pierre WARTBURG, and Michael ZEPPEZAUER. "H8Zn(c)2 and Zn(c)2Co(n)2 human liver alcohol dehydrogenase." European Journal of Biochemistry 173, no. 2 (April 1988): 281–85. http://dx.doi.org/10.1111/j.1432-1033.1988.tb13996.x.

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GABEN, A., and J. MESTER. "Balb/c 3T3 fibroblasts expressing human estrogen receptor." Cell Biology International Reports 14 (September 1990): 99. http://dx.doi.org/10.1016/0309-1651(90)90498-n.

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Sun, Guoming, Shunqian Jin, and R. Baskaran. "MMR/c-Abl-dependent activation of ING2/p73α signaling regulates the cell death response to N-methyl-N′-nitro-N-nitrosoguanidine." Experimental Cell Research 315, no. 18 (November 2009): 3163–75. http://dx.doi.org/10.1016/j.yexcr.2009.09.010.

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May, Gerhard H. W., K. Elizabeth Allen, William Clark, Martin Funk, and David A. F. Gillespie. "Analysis of the Interaction between c-Jun and c-Jun N-terminal Kinasein Vivo." Journal of Biological Chemistry 273, no. 50 (December 11, 1998): 33429–35. http://dx.doi.org/10.1074/jbc.273.50.33429.

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Wolfman, Janice C., Todd Palmby, Channing J. Der, and Alan Wolfman. "Cellular N-Ras Promotes Cell Survival by Downregulation of Jun N-Terminal Protein Kinase and p38." Molecular and Cellular Biology 22, no. 5 (March 1, 2002): 1589–606. http://dx.doi.org/10.1128/mcb.22.5.1589-1606.2002.

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ABSTRACT Cellular N-Ras provides a steady-state antiapoptotic signal, at least partially through the regulation of phosphorylated Akt and Bad levels. Fibroblasts lacking c-N-Ras expression are highly sensitive to the induction of apoptosis by a variety of agents. Reduction of pBad and pAkt levels using a phosphatidylinositol 3-kinase inhibitor was not sufficient to sensitize the control cell population to the high level of apoptosis observed in the N-Ras knockout cell lines, suggesting that c-N-Ras provides at least one other antiapoptotic signal. Stimulation of the control cells with apoptotic agents results in a transient increase in Jun N-terminal protein kinase (JNK)/p38 activity that decreased to baseline levels during the time course of the experiments. In all cases, however, sustained JNK/p38 activity was observed in cells lacking c-N-Ras expression. This correlated with sustained levels of phosphorylated MKK4 and MKK3/6, upstream activators of JNK and p38, respectively. Mimicking the sustained activation of JNK in the control cells did result in increasing their sensitivity to apoptotic agents, suggesting that prolonged JNK activity is a proapoptotic event. We also examined the potential downstream c-N-Ras targets that might be involved in regulating the duration of the JNK/p38 signal. Only the RalGDS 37G-N-Ras protein protected the N-Ras knockout cells from apoptosis and restored transient rather than sustained JNK activation. These data suggest that cellular N-Ras provides an antiapoptotic signal through at least two distinct mechanisms, one which regulates steady-state pBad and pAkt levels and one which regulates the duration of JNK/p38 activity following an apoptotic challenge.
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Dissertations / Theses on the topic "Cell biology, n.e.c"

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Lumngwena, Evelyn Ngwa. "The impact of HIV-1 subtype C Envelope N-glycosylation on DC-SIGN meditated modulation of DC function to facilitate transmission or enhance viral pathogenesis." Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/27096.

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N-glycosylation plays an important role in Envelope (Env) function and may be involved in the modulation of the immune response to HIV-1 infection. In this study, we hypothesized that Env N-glycosylation may affect viral pathogenesis by influencing Env structure and function. Furthermore, we also postulated that differences in Env glycosylation could affect interactions between Env and DC-SIGN of dendritic cells (DCs), activating alternative signalling pathways which stimulate the release of different immune modulators. We generated pseudovirus of eighteen Env clones (PSVs) with variable number and position of potential N-glycan sites (PNGs) and compared their ability to infect TZM-bl cells, bind to Raji+ DC-SIGN cells, trans-infect TZM-bl cells when captured by either Raji-DC-SIGN cells or monocyte-derived dendritic cells (MDDCs) and modulate MDDC signaling by investigating the release of Interleukin-10 (IL-10) and other immune modulatory cytokines and MAPK activation. Entry efficiency, DC-SIGN binding and trans-infection varied widely across all clones. The level of IL-10 secreted by MDDCs in response to PSV stimulation varied 32-fold. The induction of IL-10 secretion by purified gp140 confirmed that Env was the viral component that stimulated the secretion of IL-10 via interaction with DC-SIGN and potentially other undefined receptors. PSV and purified gp140 stimulated MDDC signaling via ERK and JNK phosphorylation, while p38 was not activated. The addition of recombinant DC-SIGN lowered the levels of secreted IL-10 and ERK /JNK phosphorylation, suggesting that DC-SIGN plays a role in these responses. As Env mannosylation correlated with DC-SIGN binding, five highly conserved Env PNGs (241, 262, 386, 392, and 448) previously identified to carry high mannose type N-glycans and hence thought to be involved in DC-SIGN binding were deleted in two Env clones by site-directed mutagenesis to confirm their importance in Env function. The potential role of these PNGs in Env entry efficiency, DC-SIGN binding, trans-infection, induction of MDDC IL-10 secretion and activation of MAPK phosphorylation was determined. Deletion of these sites significantly affected the entry efficiency, DC-SIGN binding, trans-infection and MDDC IL-10 secretion, with one Env clone proving to be more sensitive to mutation than the other. This suggests that PNGs influence Env function in a clone-specific manner. As deletion of highly conserved PNGs abrogated Env function we used sequence analysis to identify PNGs involved in binding DC-SIGN and inducing MDDC IL-10 secretion. We grouped PSVs based on the presence or absence of specific PNGs in Env sequences and compared entry efficiency, DC-SIGN binding, trans-infection, stimulation of MDDC IL-10 secretion and induction of MAPK phosphorylation. Three Env PNGs were significantly associated with entry efficiency (N356, N392, and N674), and three sites (N289, N356 and 674) were significantly associated with trans-infection while N674 also influenced DCSIGN binding. The majority of MDDC donors secreted higher levels of IL-10 when stimulated with PSVs that carried PNGS at N130 (p = 0.0016) and N332 (p = 0.0039) and lacked N674 (p = 0.033). When Envs were graded on whether they had 0, 1, 2 or 3 of the PNGs (e.g. -130, -332, +674; -130, +332 and +674, etc.) those that carried either one of the PNGs or the entire induction motif (N130+ N332+ N674-) significantly stimulated MDDCs to secrete higher levels of IL-10 than those that completely lacked the motif (p = 0.0335 and p = 0.0304, respectively). As the presence of N674 was linked to reduction in all functions of Env, it is likely that the presence of an N-glycan at this site affected Env structure and could skew the analysis. Excluding N674 indicated that the presence of PNGs at position 130 and 332 was sufficient to induce significantly higher IL-10 release than those that had either none or one of these sites (p = 0.0053). When we determined whether N130 and N332 were enriched in subtype C acute infection Envs, these sequences were not enriched with PNGs at either N130 or N332 compared to chronic infection viruses. However, when IL-10 levels were compared between MDDC donors stimulated with PSV of either acute or chronic infection clones, those from early infection significantly enhanced MDDC secretion of IL-10 (p = 0.0039). This suggests that even though PNGs at 130 and N332 could be involved in inducing MDDC IL-10 secretion, it is not the only requirement for enhanced stimulation. Although Env differentially activated ERK and JNK phosphorylation, ERK phosphorylation did not correlate with IL-10 secretion, suggesting that this MAPK signaling pathway was not solely responsible for triggering the release of MDDC IL-10 and other regulatory cytokines. PSVs also stimulated the release of TNFα, IL-1β, IL-6, IL-8, MIP-1a, and MIP-1b while having no effect on IL-12 levels. This suggests that HIV-1 binding to DCs in the genital tract could change the dynamics of DC immune responses, deregulating their cytokines secretion and destabilising the Th0 cell differentiation to facilitate viral survival and thus productive clinical infection. We therefore conclude that HIV-1 variants differentially stimulate MDDCs to release immunosuppressive IL-10 and that transmitted founders could be better at modulating immune responses in the genital tract compared to chronic infection variants.
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Smith, Abigail O. "Defining the Role of c-Jun N-terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1141.

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Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people. It primarily is caused by mutations in the transmembrane proteins Polycystin-1 (PKD1) and Polycystin-2 (PKD2). The most proximal effects of polycystin mutations leading to cyst formation are not known, but pro-proliferative signaling must be involved for the tubule epithelial cells to increase in number over time. The stress-activated mitogen-activated protein kinase (MAPK) pathway c-Jun N-terminal kinase (JNK) promotes proliferation in specific contexts and is activated in acute and chronic kidney disease. Previous work found evidence of JNK activation in cystic tissues (Le et al., 2005) and others showed that JNK signaling is activated by aberrant expression of PKD1 and PKD2 in cell culture (Arnould et al., 1998; Arnould et al., 1999; Parnell et al., 2002; Yu et al., 2010) but the contribution of JNK signaling to cystic disease in vivo has not been investigated. This body of work describes the use of conditional and germline deletion of Pkd2, Jnk1 and Jnk2 to model ADPKD and JNK signaling inhibition in juvenile and adult mice. Immunoblots and histological staining were used to measure JNK activation and evaluate the effect of JNK deletion on cystic disease. Results show that Pkd2 deletion activated JNK signaling in juvenile and adult mice. Reduction of JNK activity significantly reduced cystic burden in kidneys of juvenile Pkd2 mutant mice. This correlated with reduced tubule cell proliferation and reduced kidney fibrosis. The improvement in cystic phenotype was driven primarily by Jnk1 deletion rather than Jnk2. JNK signaling inhibition in adult Pkd2 mutants significantly reduced liver cysts when mice were aged six months. JNK inhibition reduces the severity of cystic disease caused by the loss of Pkd2 suggesting that the JNK pathway should be explored as a potential therapeutic target for ADPKD.
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Amin, Shahreen. "Regulation of the tyrosine phosphatase SHP-1 expression by C-jun-N-terminal kinase and RFX-1 and AP-4 transcription factors in insulin-like growth factor-1 (IGF-1) stimulated breast adenocarcinoma MCF-7 cells." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26837.

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This thesis is devoted to reveal the negative regulators in IGF-1 (Insulin like growth factor 1) stimulated growth of a human breast adenocarcinoma cell line. It is a well established fact that increased circulating levels of IGF-1 correlate with increased risk of breast cancer. IGF-1 activation of its receptor, IGF-1R, is implicated in the progression of breast cancer, where IGF-1 stimulation leads to proliferative and anti-apoptotic responses by stimulating MAPK Erk and PI3K, respectively. In this study, IGF-1 stimulated MCF-7 cells proliferated more in the absence of MAPK JNK, implicating the involvement of MAPK JNK in the negative regulation of IGF-1 stimulated cell growth. In this research study, we show for the first time that IGF-1 stimulation of breast cancer cells induces SHP-1-expression by activating JNK, which in turn, activates RFX-1 and AP-4 transcription factors to allow them to bind to the high-expression region of the SHP-1 P-1 promoter in breast adenocarcinoma MCF-7 cells. (Abstract shortened by UMI.)
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Souyri-Caporale, Michèle. "Etude du pouvoir tumorigene de l'oncogene n-ras." Paris 7, 1987. http://www.theses.fr/1987PA077083.

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Gavériaux, Claire. "Etude de l'interaction entre l'immunoglobuline e et son recepteur de forte affinite : mise au point d'un nouvel essai immunoenzymatique sur cellules, le celisa, importance de la n-glycosylation et de l'activation de la proteine kinase c dans l'expresion fonctionnelle de ce recepteur." Université Louis Pasteur (Strasbourg) (1971-2008), 1988. http://www.theses.fr/1988STR13014.

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Baalbaki, Zein El-A. "Vibrational relaxation of N₄O, C₄H₄, and C₄H₄-Ar mixtures." Thesis, University of Ottawa (Canada), 1986. http://hdl.handle.net/10393/4666.

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Lloyd-Evans, Emyr. "Cell biology of Niemann-Pick type C disease." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437185.

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Co, Carl. "N-WASP at the membrane-actin interface." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3251943.

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Angers-Loustau, Alexandre. "Roles of c-Src and hDRR1 in glioma cell invasion." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85118.

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Malignant glioma is the major brain tumor in adults, and has a poor prognosis. The failure to control invasive cell subpopulations may be the key reason for local glioma recurrence after radical tumor resection, and may contribute substantially to the failure of the other treatment modalities, such as radiation therapy and chemotherapy. As a model for this invasion, we have implanted spheroids from a human glioma cell line (U251) in three-dimensional collagen type I matrices which these cells readily invade. First, we observed that the Src family kinase specific pharmacological inhibitors PP2 and SU6656 significantly inhibited the invasion of the cells in this assay, which was then confirmed by expression of two inhibitors of Src family function, dominant inhibitory Src and CSK. Fluorescent time-lapse microscopy on U251 cells stably expressing a YFP-actin construct shows that PP2 caused the disappearance of peripheral membrane ruffles within minutes in monolayer cultures, and induced the loss of actin bursting at the leading tip of the invadopodium in three-dimensions. The inhibition of Src family activity is thus a potential therapeutic approach to treating highly invasive malignant glioma. In the second part, we analyze the role of a novel protein, hDRR1, which was cloned from a functional screen of genes involved in glioma cell hyperinvasion. We show that hDRR1 localizes endogenously and when overexpressed to the actin cytoskeleton, via two independent but homologous actin-localization domains. We also show that the C-terminus of hDRR1 can bind to the light chain of MAP1A and MAP1B, and that hDRR1 overexpression in invading glioma cells results in a decrease in the percentage of cells adopting a polarized morphology. These results suggest that hDRR1 represents a novel actin-tubulin bridging protein that plays important roles in cytoskeletal events.
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McLachlan, Ian Gordon. "Genetic control of dendrite morphogenesis in C. elegans." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493511.

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The shapes and attachments of cells determine the machinery of organs; for example, the shapes and attachments of neurons and glia establish the wiring of the brain. To understand how neuronal dendrites obtain their morphologies and make the appropriate connections, we used C. elegans sense organs as models. Previous work identified a requirement for the extracellular matrix protein DYF-7 in dendrite extension: DYF-7 anchors dendrites dendrite endings at the embryonic nose while neuronal cell bodies migrate away, and in its absence, dendrites fail to extend. Here, we show that these dendrites are part of a sensory epithelium composed of glial cells and neurons. The dendrites are ensheathed by glial cells, form adherens junctions onto glia, and are stabilized at their apical surfaces by the extracellular matrix protein DYF-7. In dyf-7 mutants, the pulling force of cell migration causes this sensory epithelium to rupture along the glia:glia junctions. By comparison, dendrites of the URX and BAG neurons are intimately connected to the external surface of glial cells but are not known to form adherens junctions and are not affected in dyf-7 mutants. To identify factors required for URX and BAG dendrite extension, we performed forward genetic screens for dendrite extension defects in these cells and identified mutations in the cytoplasmic protein GRDN-1/Girdin and the adhesion molecule SAX-7/L1CAM. We show that in wild-type embryos, URX and BAG dendrites also extend by attaching to the nose and then stretching during embryo elongation but, in grdn-1 embryos, they fail to remain attached. GRDN-1 can promote dendrite attachment by acting in glia—it localizes to glial endings and causes localized accumulation of SAX-7, creating an adhesive compartment where dendrites attach. Thus, GRDN-1 and SAX-7 determine dendrite length by positioning a neuron-glia attachment site that couples dendrite extension to embryonic growth. Finally, we identified several other mutants with URX dendrite morphogenesis defects, including overgrowth of the URX dendrite; some have been mapped to genes associated with the cytoskeleton. Together, these studies define genetic mechanisms that control morphogenesis of distinct classes of sensory dendrites through specific adhesive interactions with their glial neighbors.
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Books on the topic "Cell biology, n.e.c"

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1962-, Li Min, ed. NMDA receptor protocols. Totowa, N.J: Humana Press, 1999.

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Micropatterning in Cell Biology Part C. Elsevier, 2014. http://dx.doi.org/10.1016/c2013-0-09944-6.

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Piel, Matthieu, and Manuel Théry. Micropatterning in Cell Biology, Part C. Elsevier Science & Technology Books, 2014.

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R, Harris James, ed. Ascorbic acid: Biochemistry and biomedical cell biology. New York: Plenum Press, 1996.

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Guthrie, Christine, and Gerald R. Fink. Guide to Yeast Genetics and Molecular and Cell Biology, Part C. Elsevier Science & Technology Books, 2002.

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Guthrie, Christine, and Gerald R. Fink. Guide to Yeast Genetics and Molecular and Cell Biology, Part C. Elsevier Science & Technology Books, 2002.

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Germ Cell Development in C Elegans Advances in Experimental Medicine and Biology. Springer, 2012.

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Microfluidics in Cell Biology Part C: Microfluidics for Cellular and Subcellular Analysis. Elsevier, 2018. http://dx.doi.org/10.1016/s0091-679x(18)x0004-1.

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Fletcher, Daniel, Matthieu Piel, and Junsang Doh. Microfluidics in Cell Biology Part C: Microfluidics for Cellular and Subcellular Analysis. Elsevier Science & Technology, 2018.

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KARP. Website to Accompany Cell and Molecular Biology: C Oncepts and Experiments, Third Edition. John Wiley & Sons Inc, 2002.

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Book chapters on the topic "Cell biology, n.e.c"

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Maclean, Norman. "N." In Macmillan Dictionary of Genetics and Cell Biology, 267–80. London: Macmillan Education UK, 1987. http://dx.doi.org/10.1007/978-1-349-18905-2_14.

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Maclean, Norman. "C." In Macmillan Dictionary of Genetics and Cell Biology, 55–106. London: Macmillan Education UK, 1987. http://dx.doi.org/10.1007/978-1-349-18905-2_3.

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Veit, Christiane, Ulrike Vavra, and Richard Strasser. "N-Glycosylation and Plant Cell Growth." In Methods in Molecular Biology, 183–94. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1902-4_16.

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Sato, Yoji, Albrecht G. Schmidt, Helen Kiriazis, Brian D. Hoit, and Evangelia G. Kranias. "Compensated hypertrophy of cardiac ventricles in aged transgenic FVB/N mice overexpressing calsequestrin." In Cardiac Cell Biology, 19–25. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-4712-6_3.

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Bayer, Allison L., Maria C. Heidkamp, Nehu Patel, Michael Porter, Steve Engman, and Allen M. Samarel. "Alterations in protein kinase C isoenzyme expression and autophosphorylation during the progression of pressure overload-induced left ventricular hypertrophy." In Cardiac Cell Biology, 145–52. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-4712-6_19.

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Varshavsky, A., C. Byrd, I. V. Davydov, R. J. Dohmen, F. Du, M. Ghislain, M. Gonzalez, et al. "The N-End Rule Pathway." In Ubiquitin and the Biology of the Cell, 223–78. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1922-9_8.

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Cote, Gilbert J., Elizabeth G. Grubbs, and Marie-Claude Hofmann. "Thyroid C-Cell Biology and Oncogenic Transformation." In Medullary Thyroid Carcinoma, 1–39. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22542-5_1.

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Yong, V. W., and L. Y. S. Oh. "Protein Kinase C Regulates Process Formation by Oligodendrocytes." In Cell Biology and Pathology of Myelin, 173–85. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5949-8_18.

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de la Fuente, Cynthia, and Maria Teresa Catanese. "Production and Purification of Cell Culture Hepatitis C Virus." In Methods in Molecular Biology, 105–19. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8976-8_7.

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Crittenden, Sarah L., Hannah S. Seidel, and Judith Kimble. "Analysis of the C. elegans Germline Stem Cell Pool." In Methods in Molecular Biology, 1–33. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-4017-2_1.

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Conference papers on the topic "Cell biology, n.e.c"

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"Application of single-cell Hi-C method for analysis of lampbrush chromosome сonformation." In SYSTEMS BIOLOGY AND BIOINFORMATICS (SBB-2020). Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences., 2020. http://dx.doi.org/10.18699/sbb-2020-27.

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Hsieh, Po-Tsung, Ming-Hsien Li, Wei-Chiao Hung, Chia-Ming Yang, Peter Chen, and In-Gann Chen. "Large Area (>1cm2) Efficient Perovskite/N type C-Si Tandem Solar Cell." In 2020 IEEE 47th Photovoltaic Specialists Conference (PVSC). IEEE, 2020. http://dx.doi.org/10.1109/pvsc45281.2020.9300472.

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Mikolasek, M., M. Nemec, J. Kovac, G. Mannino, C. Gerardi, C. Tringali, L. Harmatha, and S. Lombardo. "Electrical characterisation of a-Si:H(n)/c-Si(p) heterostructures for solar cell applications." In 2012 International Conference on Advanced Semiconductor Devices & Microsystems (ASDAM). IEEE, 2012. http://dx.doi.org/10.1109/asdam.2012.6418543.

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Verma, Manish, and Guru Prasad Mishra. "Ta2O5 as Tunneling Oxide for n-type Passivated c-Si CS-TOPCon Solar Cell." In 2021 Devices for Integrated Circuit (DevIC). IEEE, 2021. http://dx.doi.org/10.1109/devic50843.2021.9455930.

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Chu, C. Y., C. Y. Chang, and W. F. Su. "(Invited) Low Temperature Solution Processable n-i-p Perovskite Solar Cell." In 2015 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2015. http://dx.doi.org/10.7567/ssdm.2015.c-1-2.

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Kumar, Raj, Ørnulf Nordseth, Geraldo Cristian Vásquez, Sean Erik Foss, Eduard Monakhov, and Bengt Gunnar Svensson. "Investigation of n-Al:ZnO/p-Cu2O heterojunction for c-Si tandem heterojunction solar cell applications." In 15th International Conference on Concentrator Photovoltaic Systems (CPV-15). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5123885.

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Izzi, M., L. Serenelli, P. Mangiapane, E. Salza, M. Tucci, M. Delia Noce, I. Usatii, et al. "Relevance Of TCO workfunction in n-silicon oxide emitter - c-Si (p) heterojunction solar cell." In 2015 IEEE 42nd Photovoltaic Specialists Conference (PVSC). IEEE, 2015. http://dx.doi.org/10.1109/pvsc.2015.7356055.

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Blanco, Idoia, Paula Lazcoz, Jon Celay, Xing Fan, Javier S. Castresana, and Ignacio J. Encio. "Abstract 3663: Effects of chemotherapy on cell survival, cell cycle biology and apoptosis in the SK-N-FI neuroblastoma cell line." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3663.

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Yurlova, Larisa, Andrea Buchfellner, Jacqueline Gregor, Tina Romer, and Ian Hickson. "Abstract 86: Live-cell profiling of inhibitors targeting the N/C interaction within the androgen receptor." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-86.

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Hadi, Sabina Abdul, Ayman Rizk, and Ammar Nayfeh. "Effects of 2.85 nm Si Nanoparticles on AZO/n+/p c-Si Thin Film Solar Cell." In 2020 IEEE 47th Photovoltaic Specialists Conference (PVSC). IEEE, 2020. http://dx.doi.org/10.1109/pvsc45281.2020.9300420.

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Reports on the topic "Cell biology, n.e.c"

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Delmer, Deborah P., Douglas Johnson, and Alex Levine. The Role of Small Signal Transducing Gtpases in the Regulation of Cell Wall Deposition Patterns in Plants. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570571.bard.

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The combined research of the groups of Delmer, Levine and Johnson has led to a number of interesting findings with respect to the function of the small GTPase Rac in plants and also opened up new leads for future research. The results have shown: 1) The Rac13 protein undergoes geranylgeranlyation and is also translocated to the plasma membrane as found for Rac in mammals; 2) When cotton Rac13 is highly- expressed in yeast, it leads to an aberrant phenotype reminiscent of mutants impaired in actin function, supporting a role for Rac13 in cytoskeletal organization; 3) From our searches, there is no strong evidence that plants contain homologs of the related CDC42 genes found in yeast and mammals; 4) We have identified a rather unique Rac gene in Arabidopsis that has unusual extensions at both the N- and C-terminal portions of the protein; 5) New evidence was obtained that an oxidative burst characterized by substantial and sustained production of H202 occurs coincident with the onset of secondary wall synthesis in cotton fibers. Further work indicates that the H202 produced may be a signal for the onset of this phase of development and also strongly suggests that Rac plays an important role in signaling for event. Since the secondary walls of plants that contain high levels of lignin and cellulose are the major source of biomass on earth, understanding what signals control this process may well in the future have important implications for manipulating the timing and extent of secondary wall deposition. 6) When the cotton Rac13 promoter is fused to the reporter gene GUS, expression patterns in Arabidopsis indicate very strong and specific expression in developing trichomes and in developing xyelm. Since both of these cell types are engaged in secondary wall synthesis, this further supports a role for Rac in signaling for onset of this process. Since cotton fibers are anatomically defined as trichomes, these data may also be quite useful for future studies in which the trichomes of Arabidopsis may serve as a model for cotton fiber development; the Rac promoter can therefore be useful to drive expression of other genes proposed to affect fiber development and study the effects on the process; 7) The Rac promoter has also been shown to be the best so far tested for use in development of a system for transient transformation of developing cotton fibers, a technique that should have many applications in the field of cotton biotechnology; 8) One candidate protein that may interact with Rac13 to be characterized further in the future is a protein kinase that may be analogous to the PAK kinase that is known to interact with Rac in mammals.
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Palmer, Guy, Varda Shkap, Wendy Brown, and Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, March 2007. http://dx.doi.org/10.32747/2007.7695879.bard.

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Anaplasmosis an arthropod-born disease of cattle caused by the rickettsia Anaplasma marginale and is an impediment to efficient production of healthy livestock in both Israel and the United States. Currently the only effective vaccines are derived from the blood of infected cattle. The risk of widespread transmission of both known and newly emergent pathogens has prevented licensure of live blood-based vaccines in the U.S. and is a major concern for their continued use in Israel. Consequently development of a safe, effective vaccine is a high priority. In this collaborative project we focused on two approaches to vaccine development. The first focused o n improving antigen delivery to livestock and specifically examined how DNA vaccines could be improved to enhance priming and expansion of the immune response. This research resulted in development and testing of two novel vaccine delivery systems--one that targeted antigen spread among dendritic cells (the key cell in priming immune responses and a follow-on construct that also specifically targeted antigen to the endosomal-lysosomal compartment the processing organelle within the dendritic cell that directs vaccine antigen to the MHC class ll-CD4* T cell priming pathway). The optimized construct targeting vaccine antigen to the dendritic cell MHC class II pathway was tested for ability to prime A. marginale specific immune responses in outbred cattle. The results demonstrated both statistically significant effects of priming with a single immunization, continued expansion of the primary immune response including development of high affinity lgG antibodies and rapid recall of the memory response following antigen challenge. This portion of the study represented a significant advance in vaccine delivery for livestock. Importantly the impact of these studies is not limited to A. marginale a s the targeting motifs are optimized for cattle and can be adapted to other cattle vaccinations by inserting a relevant pathogen-specific antigen. The second approach (which represented an addition to the project for which approval was requested as part of the first annual report) was a comparative approach between A . marginale and the Israel A . centrale vaccines train. This addition was requested as studies on Major Surface Protein( MSP)- 2 have shown that this antigen is highly antigenically variable and presented solely as a "static vaccine" antigen does not give cross-strain immunity. In contrast A. . centrale is an effective vaccine which Kimron Veterinary institute has used in the field in Israel for over 50 years. Taking advantage of this expertise, a broad comparison of wild type A. marginale and vaccine strain was initiated. These studies revealed three primary findings: i) use of the vaccine is associated with superinfection, but absence of clinical disease upon superinfection with A. marginale; ii) the A. centrale vaccine strain is not only less virulent but transmission in competent in Dermacentor spp. ticks; and iii) some but not all MSPs are conserved in basic orthologous structure but there are significant polymorphisms among the strains. These studies clearly indicated that there are statistically significant differences in biology (virulence and transmission) and provide a clear path for mapping of biology with the genomes. Based on these findings, we initiated complete genome sequencing of the Israel vaccine strain (although not currently funded by BARD) and plant to proceed with a comparative genomics approach using already sequenced wild-type A. marginale. These findings and ongoing collaborative research tie together filed vaccine experience with new genomic data, providing a new approach to vaccine development against a complex pathogen.
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Droby, Samir, Michael Wisniewski, Martin Goldway, Wojciech Janisiewicz, and Charles Wilson. Enhancement of Postharvest Biocontrol Activity of the Yeast Candida oleophila by Overexpression of Lytic Enzymes. United States Department of Agriculture, November 2003. http://dx.doi.org/10.32747/2003.7586481.bard.

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Enhancing the activity of biocontrol agents could be the most important factor in their success in controlling fruit disease and their ultimate acceptance in commercial disease management. Direct manipulation of a biocontrol agent resulting in enhancement of diseases control could be achieved by using recent advances in molecular biology techniques. The objectives of this project were to isolate genes from yeast species that were used as postharvest biocontrol agents against postharvest diseases and to determine their role in biocontrol efficacy. The emphasis was to be placed on the yeast, Candida oleophila, which was jointly discovered and developed in our laboratories, and commercialized as the product, Aspire. The general plan was to develop a transformation system for C . oleophila and either knockout or overexpress particular genes of interest. Additionally, biochemical characterization of the lytic peptides was conducted in the wild-type and transgenic isolates. In addition to developing a better understanding of the mode of action of the yeast biocontrol agents, it was also our intent to demonstrate the feasibility of enhancing biocontrol activity via genetic enhancement of yeast with genes known to code for proteins with antimicrobial activity. Major achievements are: 1) Characterization of extracellular lytic enzymes produced by the yeast biocontrol agent Candida oleophila; 2) Development of a transformation system for Candida oleophila; 3) Cloning and analysis of C.oleophila glucanase gene; 4) Overexpression of and knockout of C. oleophila glucanase gene and evaluating its role in the biocontrol activity of C. oleophila; 5) Characterization of defensin gene and its expression in the yeast Pichiapastoris; 6) Cloning and Analysis of Chitinase and Adhesin Genes; 7) Characterization of the rnase secreted by C . oleophila and its inhibitory activity against P. digitatum. This project has resulted in information that enhanced our understanding of the mode of action of the yeast C . oleophila. This was important step towards enhancing the biocontrol activity of the yeast. Fungal cell wall enzymes produced by the yeast antagonist were characterized. Different substrates were identified to enhance there production in vitro. Exo-b-1, 3 glucanase, chitinase and protease production was stimulated by the presence of cell-wall fragments of Penicillium digitatum in the growing medium, in addition to glucose. A transformation system developed was used to study the role of lytic enzymes in the biocontrol activity of the yeast antagonist and was essential for genetic manipulation of C . oleqphila. After cloning and characterization of the exo-glucanase gene from the yeast, the transformation system was efficiently used to study the role of the enzyme in the biocontrol activity by over-expressing or knocking out the activity of the enzyme. At the last phase of the research (still ongoing) the transformation system is being used to study the role of chitinase gene in the mode of action. Knockout and over expression experiments are underway.
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Sessa, Guido, and Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7699834.bard.

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The research problem: Pseudomonas syringae pv. tomato (Pst) and Xanthomonas campestrispv. vesicatoria (Xcv) are the causal agents of tomato bacterial speck and spot diseases, respectively. These pathogens colonize the aerial parts of the plant and cause economically important losses to tomato yield worldwide. Control of speck and spot diseases by cultural practices or chemicals is not effective and genetic sources of resistance are very limited. In previous research supported by BARD, by gene expression profiling we identified signaling components involved in resistance to Xcvstrains. Follow up experiments revealed that a tomato gene encoding a MAP kinase kinase kinase (MAPKKKe) is required for resistance to Xcvand Pststrains. Goals: Central goal of this research was to investigate the molecular mechanisms by which MAPKKKεand associated MAP kinase cascades regulate host resistance. Specific objectives were to: 1. Determine whether MAPKKKεplays a broad role in defense signaling in plants; 2. Identify components of MAP kinase cascades acting downstream of MAPKKKε; 3. Determine the role of phosphorylation-related events in the function of MAPKKKε; 4. Isolate proteins directly activated by MAPKKKε-associatedMAPK modules. Our main achievements during this research program are in the following major areas: 1. Characterization of MAPKKKεas a positive regulator of cell death and dissection of downstream MAP kinase cascades (Melech-Bonfil et al., 2010; Melech-Bonfil and Sessa, 2011). The MAPKKKεgene was found to be required for tomato resistance to Xcvand Pstbacterial strains and for hypersensitive response cell death triggered by different R gene/effector gene pairs. In addition, overexpression analysis demonstrated that MAPKKKεis a positive regulator of cell death, whose activity depends on an intact kinase catalytic domain. Epistatic experiments delineated a signaling cascade downstream of MAPKKKεand identified SIPKK as a negative regulator of MAPKKKε-mediated cell death. Finally, genes encoding MAP kinase components downstream of MAPKKKεwere shown to contribute to tomato resistance to Xcv. 2. Identification of tomato proteins that interact with MAPKKKεand play a role in plant immunity (Oh et al., 2011). We identified proteins that interact with MAPKKKε. Among them, the 14-3-3 protein TFT7 was required for cell death mediated by several R proteins. In addition, TFT7 interacted with the MAPKK SlMKK2 and formed homodimersin vivo. Thus, TFT7 is proposed to recruit SlMKK2 and MAPKKK client proteins for efficient signal transfer. 3. Development of a chemical genetic approach to identify substrates of MAPKKKε-activated MAP kinase cascades (Salomon et al., 2009, 2011). This approach is based on engineering the kinase of interest to accept unnatural ATP analogs. For its implementation to identify substrates of MAPKKKε-activated MAP kinase modules, we sensitized the tomato MAP kinase SlMPK3 to ATP analogs and verified its ability to use them as phosphodonors. By using the sensitized SlMPK3 and radiolabeled N6(benzyl)ATP it should be possible to tag direct substrates of this kinase. 4. Development of methods to study immunity triggered by pathogen-associated molecular patterns (PAMPs) in tomato and N. benthamiana plants (Kim et al., 2009; Nguyen et al. 2010). We developed protocols for measuring various PTI-associatedphenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition at the cell wall, activation of MAP kinases, and a luciferase-based reporter system for use in protoplasts. Scientific and agricultural significance: Our research activities discovered and characterized a signal transduction pathway mediating plant immunity to bacterial pathogens. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease. In addition, we successfully developed new biochemical and molecular methods that can be implemented in the study of plant immunity and other aspects of plant biology.
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Epel, Bernard, and Roger Beachy. Mechanisms of intra- and intercellular targeting and movement of tobacco mosaic virus. United States Department of Agriculture, November 2005. http://dx.doi.org/10.32747/2005.7695874.bard.

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To cause disease, plant viruses must replicate and spread locally and systemically within the host. Cell-to-cell virus spread is mediated by virus-encoded movement proteins (MPs), which modify the structure and function of plasmodesmata (Pd), trans-wall co-axial membranous tunnels that interconnect the cytoplasm of neighboring cells. Tobacco mosaic virus (TMV) employ a single MP for cell- cell spread and for which CP is not required. The PIs, Beachy (USA) and Epel (Israel) and co-workers, developed new tools and approaches for study of the mechanism of spread of TMV that lead to a partial identification and molecular characterization of the cellular machinery involved in the trafficking process. Original research objectives: Based on our data and those of others, we proposed a working model of plant viral spread. Our model stated that MPᵀᴹⱽ, an integral ER membrane protein with its C-terminus exposed to the cytoplasm (Reichel and Beachy, 1998), alters the Pd SEL, causes the Pd cytoplasmic annulus to dilate (Wolf et al., 1989), allowing ER to glide through Pd and that this gliding is cytoskeleton mediated. The model claimed that in absence of MP, the ER in Pd (the desmotubule) is stationary, i.e. does not move through the Pd. Based on this model we designed a series of experiments to test the following questions: -Does MP potentiate ER movement through the Pd? - In the presence of MP, is there communication between adjacent cells via ER lumen? -Does MP potentiate the movement of cytoskeletal elements cell to cell? -Is MP required for cell-to-cell movement of ER membranes between cells in sink tissue? -Is the binding in situ of MP to RNA specific to vRNA sequences or is it nonspecific as measured in vitro? And if specific: -What sequences of RNA are involved in binding to MP? And finally, what host proteins are associated with MP during intracellular targeting to various subcellular targets and what if any post-translational modifications occur to MP, other than phosphorylation (Kawakami et al., 1999)? Major conclusions, solutions and achievements. A new quantitative tool was developed to measure the "coefficient of conductivity" of Pd to cytoplasmic soluble proteins. Employing this tool, we measured changes in Pd conductivity in epidermal cells of sink and source leaves of wild-type and transgenic Nicotiana benthamiana (N. benthamiana) plants expressing MPᵀᴹⱽ incubated both in dark and light and at 16 and 25 ᵒC (Liarzi and Epel, 2005 (appendix 1). To test our model we measured the effect of the presence of MP on cell-to-cell spread of a cytoplasmic fluorescent probe, of two ER intrinsic membrane protein-probes and two ER lumen protein-probes fused to GFP. The effect of a mutant virus that is incapable of cell-to-cell spread on the spread of these probes was also determined. Our data shows that MP reduces SEL for cytoplasmic molecules, dilates the desmotubule allowing cell-cell diffusion of proteins via the desmotubule lumen and reduces the rate of spread of the ER membrane probes. Replicase was shown to enhance cell-cell spread. The data are not in support of the proposed model and have led us to propose a new model for virus cell-cell spread: this model proposes that MP, an integral ER membrane protein, forms a MP:vRNAER complex and that this ER-membrane complex diffuses in the lipid milieu of the ER into the desmotubule (the ER within the Pd), and spreads cell to cell by simple diffusion in the ER/desmotubule membrane; the driving force for spread is the chemical potential gradient between an infected cell and contingent non-infected neighbors. Our data also suggests that the virus replicase has a function in altering the Pd conductivity. Transgenic plant lines that express the MP gene of the Cg tobamovirus fused to YFP under the control the ecdysone receptor and methoxyfenocide ligand were generated by the Beachy group and the expression pattern and the timing and targeting patterns were determined. A vector expressing this MPs was also developed for use by the Epel lab . The transgenic lines are being used to identify and isolate host genes that are required for cell-to-cell movement of TMV/tobamoviruses. This line is now being grown and to be employed in proteomic studies which will commence November 2005. T-DNA insertion mutagenesis is being developed to identify and isolate host genes required for cell-to-cell movement of TMV.
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Dickman, Martin B., and Oded Yarden. Genetic and chemical intervention in ROS signaling pathways affecting development and pathogenicity of Sclerotinia sclerotiorum. United States Department of Agriculture, July 2015. http://dx.doi.org/10.32747/2015.7699866.bard.

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Abstract: The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotior11111. The focus in this project was on the elucidation of the signaling events and environmental cues involved in the regulation of these processes, utilizing and continuously developing tools our research groups have established and/or adapted for analysis of S. sclerotiorum, Our stated objectives: To take advantage of the recent conceptual (ROS/PPs signaling) and technical (amenability of S. sclerotiorumto manipulations coupled with chemical genomics and next generation sequencing) developments to address and extend our fundamental and potentially applicable knowledge of the following questions concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum: (i) How do defects in genes involved in ROS signaling affect S. sclerotiorumdevelopment and pathogenicity? (ii) In what manner do phosphotyrosinephosphatases affect S. sclerotiorumdevelopment and pathogenicity and how are they linked with ROS and other signaling pathways? And (iii) What is the nature of activity of newly identified compounds that affect S. sclerotiori,111 growth? What are the fungal targets and do they interfere with ROS signaling? We have met a significant portion of the specific goals set in our research project. Much of our work has been published. Briefly. we can summarize that: (a) Silencing of SsNox1(NADPHoxidase) expression indicated a central role for this enzyme in both virulence and pathogenic development, while inactivation of the SsNox2 gene resulted in limited sclerotial development, but the organism remained fully pathogenic. (b) A catalase gene (Scatl), whose expression was highly induced during host infection is involved in hyphal growth, branching, sclerotia formation and infection. (c) Protein tyrosine phosphatase l (ptpl) is required for sclerotial development and is involved in fungal infection. (d) Deletion of a superoxidedismutase gene (Sssodl) significantly reduced in virulence on both tomato and tobacco plants yet pathogenicity was mostly restored following supplementation with oxalate. (e) We have participated in comparative genome sequence analysis of S. sclerotiorumand B. cinerea. (f) S. sclerotiorumexhibits a potential switch between biotrophic and necrotrophic lifestyles (g) During plant­ microbe interactions cell death can occur in both resistant and susceptible events. Non­ pathogenic fungal mutants S. sclerotior111n also cause a cell death but with opposing results. We investigated PCD in more detail and showed that, although PCD occurs in both circumstances they exhibit distinctly different features. The mutants trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive (resistant) response. Using electron and fluorescence microscopy, chemical effectors and reverse genetics, we have established that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this interaction Thus the control of cell death, dictated by the plant (autophagy) סr the fungus (apoptosis), is decisive to the outcome of certain plant­ microbe interactions. In addition to the time and efforts invested towards reaching the specific goals mentioned, both Pls have initiated utilizing (as stated as an objective in our proposal) state of the art RNA-seq tools in order to harness this technology for the study of S. sclerotiorum. The Pls have met twice (in Israel and in the US), in order to discuss .נחd coordinate the research efforts. This included a working visit at the US Pls laboratory for performing RNA-seq experiments and data analysis as well as working on a joint publication (now published). The work we have performed expands our understanding of the fundamental biology (developmental and pathogenic) of S. sclerotioז111וז. Furthermore, based on our results we have now reached the conclusion that this fungus is not a bona fide necrotroph, but can also display a biotrophic lifestyle at the early phases of infection. The data obtained can eventually serve .נ basis of rational intervention with the disease cycle of this pathogen.
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Ehrlich, Marcelo, John S. Parker, and Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

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Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizootic Hemorrhagic Disease Virus (EHDV) in Israel, underscore the need for: (i) a better comprehension of the infection process of orbiviruses, (ii) the identification of unique vs. common traits among different orbiviruses, (iii) the development of novel diagnosis and treatment techniques and approaches; all aimed at the achievement of more effective control and treatment measures. It is the context of these broad goals that the present project was carried out. To fulfill our long-term goal of identifying specific viral determinants of virulence, growth, and transmission of the orbiviruses, we proposed to: (i) develop reverse genetics systems for BTV and EHDV2-Ibaraki; and (ii) identify the molecular determinants of the NS3 nonstructural protein related to viroporin/viral egress activities. The first objective was pursued with a two-pronged approach: (i) development of a plasmid-based reverse genetics system for BTV-17, and (ii) development of an "in-vitro" transcription-based reverse genetics system for EHDV2-Ibaraki. Both approaches encountered technical problems that hampered their achievement. However, dissection of the possible causes of the failure to achieve viral spread of EHDV2-Ibaraki, following the transfection of in-vitro transcribed genomic segments of the virus, revealed a novel characteristic of EHDV2-Ibaraki infection: an uncharacteristically low fold increase in titer upon infection of different cell models. To address the function and regulation of NS3 we employed the following approaches: (i) development (together with Anima Cell Metrology) of a novel technique (based on the transfection of fluorescently-labeledtRNAs) that allows for the detection of the levels of synthesis of individual viral proteins (i.e. NS3) in single cells; (ii) development of a siRNA-mediated knockdown approach for the reduction in levels of expression of NS3 in EHDV2-Ibaraki infected cells; (iii) biochemical and microscopy-based analysis of the localization, levels and post-translational modifications of NS3 in infected cells. In addition, we identified the altered regulation and spatial compartmentalization of protein synthesis in cells infected with EHDV2-Ibaraki or the mammalian reovirus. In EHDV2-Ibaraki-infected cells such altered regulation in protein synthesis occurs in the context of a cell stress reponse that includes the induction of apoptosis, autophagy and activation of the stressrelated kinase c-Jun N-terminal Kinase (JNK). Interestingly, inhibition of such stress-related cellular processes diminishes the production of infectious virions, suggesting that EHDV usurps these responses for the benefit of efficient infection. Taken together, while the present project fell short of the generation of novel reverse genetics systems for orbiviruses, the development of novel experimental approaches and techniques, and their employment in the analysis of EHDV-infected cells, yielded novel insights in the interactions of orbiviruses with mammalian cells.
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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.
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