114 research outputs found

    Relationship between obesity, ethnicity and risk of late stillbirth: a case control study

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    <p>Abstract</p> <p>Background</p> <p>In high income countries there has been little improvement in stillbirth rates over the past two decades. Previous studies have indicated an ethnic disparity in the rate of stillbirths. This study aimed to determine whether maternal ethnicity is independently associated with late stillbirth in New Zealand.</p> <p>Methods</p> <p>Cases were women with a singleton, late stillbirth (≥28 weeks' gestation) without congenital abnormality, born between July 2006 and June 2009 in Auckland, New Zealand. Two controls with ongoing pregnancies were randomly selected at the same gestation at which the stillbirth occurred. Women were interviewed in the first few weeks following stillbirth, or at the equivalent gestation for controls. Detailed demographic data were recorded. The study was powered to detect an odds ratio of 2, with a power of 80% at the 5% level of significance, given a prevalence of the risk factor of 20%. A multivariable regression model was developed which adjusted for known risk factors for stillbirth, as well as significant risk factors identified in the current study, and adjusted odds ratios and 95% confidence intervals were calculated.</p> <p>Results</p> <p>155/215 (72%) cases and 310/429 (72%) controls consented. Pacific ethnicity, overweight and obesity, grandmultiparity, not being married, not being in paid work, social deprivation, exposure to tobacco smoke and use of recreational drugs were associated with an increased risk of late stillbirth in univariable analysis. Maternal overweight and obesity, nulliparity, grandmultiparity, not being married and not being in paid work were independently associated with late stillbirth in multivariable analysis, whereas Pacific ethnicity was no longer significant (adjusted Odds Ratio 0.99; 0.51-1.91).</p> <p>Conclusions</p> <p>Pacific ethnicity was not found to be an independent risk factor for late stillbirth in this New Zealand study. The disparity in stillbirth rates between Pacific and European women can be attributed to confounding factors such as maternal obesity and high parity.</p

    Diversity of isoprene-degrading bacteria in phyllosphere and soil communities from a high isoprene-emitting environment: a Malaysian oil palm plantation

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    Background: Isoprene is the most abundantly produced biogenic volatile organic compound (BVOC) on Earth, with annual global emissions almost equal to those of methane. Despite its importance in atmospheric chemistry and climate, little is known about the biological degradation of isoprene in the environment. The largest source of isoprene is terrestrial plants, and oil palms, the cultivation of which is expanding rapidly, are among the highest isoprene-producing trees. Results: DNA stable isotope probing (DNA-SIP) to study the microbial isoprene-degrading community associated with oil palm trees revealed novel genera of isoprene-utilising bacteria including Novosphingobium, Pelomonas, Rhodoblastus, Sphingomonas and Zoogloea in both oil palm soils and on leaves. Amplicon sequencing of isoA genes, which encode the α-subunit of the isoprene monooxygenase (IsoMO), a key enzyme in isoprene metabolism, confirmed that oil palm trees harbour a novel diversity of isoA sequences. In addition, metagenome assembled genomes (MAGs) were reconstructed from oil palm soil and leaf metagenomes and putative isoprene degradation genes were identified. Analysis of unenriched metagenomes showed that isoA-containing bacteria are more abundant in soils than in the oil palm phyllosphere. Conclusion: This study greatly expands the known diversity of bacteria that can metabolise isoprene and contributes to a better understanding of the biological degradation of this important but neglected climate-active gas

    The genetic epidemiology of joint shape and the development of osteoarthritis

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    Congruent, low-friction relative movement between the articulating elements of a synovial joint is an essential pre-requisite for sustained, efficient, function. Where disorders of joint formation or maintenance exist, mechanical overloading and osteoarthritis (OA) follow. The heritable component of OA accounts for ~ 50% of susceptible risk. Although almost 100 genetic risk loci for OA have now been identified, and the epidemiological relationship between joint development, joint shape and osteoarthritis is well established, we still have only a limited understanding of the contribution that genetic variation makes to joint shape and how this modulates OA risk. In this article, a brief overview of synovial joint development and its genetic regulation is followed by a review of current knowledge on the genetic epidemiology of established joint shape disorders and common shape variation. A summary of current genetic epidemiology of OA is also given, together with current evidence on the genetic overlap between shape variation and OA. Finally, the established genetic risk loci for both joint shape and osteoarthritis are discussed

    Abrolhos Bank Reef Health Evaluated by Means of Water Quality, Microbial Diversity, Benthic Cover, and Fish Biomass Data

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    The health of the coral reefs of the Abrolhos Bank (southwestern Atlantic) was characterized with a holistic approach using measurements of four ecosystem components: (i) inorganic and organic nutrient concentrations, [1] fish biomass, [1] macroalgal and coral cover and (iv) microbial community composition and abundance. The possible benefits of protection from fishing were particularly evaluated by comparing sites with varying levels of protection. Two reefs within the well-enforced no-take area of the National Marine Park of Abrolhos (Parcel dos Abrolhos and California) were compared with two unprotected coastal reefs (Sebastião Gomes and Pedra de Leste) and one legally protected but poorly enforced coastal reef (the “paper park” of Timbebas Reef). The fish biomass was lower and the fleshy macroalgal cover was higher in the unprotected reefs compared with the protected areas. The unprotected and protected reefs had similar seawater chemistry. Lower vibrio CFU counts were observed in the fully protected area of California Reef. Metagenome analysis showed that the unprotected reefs had a higher abundance of archaeal and viral sequences and more bacterial pathogens, while the protected reefs had a higher abundance of genes related to photosynthesis. Similar to other reef systems in the world, there was evidence that reductions in the biomass of herbivorous fishes and the consequent increase in macroalgal cover in the Abrolhos Bank may be affecting microbial diversity and abundance. Through the integration of different types of ecological data, the present study showed that protection from fishing may lead to greater reef health. The data presented herein suggest that protected coral reefs have higher microbial diversity, with the most degraded reef (Sebastião Gomes) showing a marked reduction in microbial species richness. It is concluded that ecological conditions in unprotected reefs may promote the growth and rapid evolution of opportunistic microbial pathogens

    Genome-wide meta-analysis of 158,000 individuals of European ancestry identifies three loci associated with chronic back pain

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    Back pain is the #1 cause of years lived with disability worldwide, yet surprisingly little is known regarding the biology underlying this symptom. We conducted a genome-wide association study (GWAS) meta-analysis of ch

    Investigating the relationships between unfavourable habitual sleep and metabolomic traits:evidence from multi-cohort multivariable regression and Mendelian randomization analyses

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    BACKGROUND: Sleep traits are associated with cardiometabolic disease risk, with evidence from Mendelian randomization (MR) suggesting that insomnia symptoms and shorter sleep duration increase coronary artery disease risk. We combined adjusted multivariable regression (AMV) and MR analyses of phenotypes of unfavourable sleep on 113 metabolomic traits to investigate possible biochemical mechanisms linking sleep to cardiovascular disease.METHODS: We used AMV (N = 17,368) combined with two-sample MR (N = 38,618) to examine effects of self-reported insomnia symptoms, total habitual sleep duration, and chronotype on 113 metabolomic traits. The AMV analyses were conducted on data from 10 cohorts of mostly Europeans, adjusted for age, sex, and body mass index. For the MR analyses, we used summary results from published European-ancestry genome-wide association studies of self-reported sleep traits and of nuclear magnetic resonance (NMR) serum metabolites. We used the inverse-variance weighted (IVW) method and complemented this with sensitivity analyses to assess MR assumptions.RESULTS: We found consistent evidence from AMV and MR analyses for associations of usual vs. sometimes/rare/never insomnia symptoms with lower citrate (- 0.08 standard deviation (SD)[95% confidence interval (CI) - 0.12, - 0.03] in AMV and - 0.03SD [- 0.07, - 0.003] in MR), higher glycoprotein acetyls (0.08SD [95% CI 0.03, 0.12] in AMV and 0.06SD [0.03, 0.10) in MR]), lower total very large HDL particles (- 0.04SD [- 0.08, 0.00] in AMV and - 0.05SD [- 0.09, - 0.02] in MR), and lower phospholipids in very large HDL particles (- 0.04SD [- 0.08, 0.002] in AMV and - 0.05SD [- 0.08, - 0.02] in MR). Longer total sleep duration associated with higher creatinine concentrations using both methods (0.02SD per 1 h [0.01, 0.03] in AMV and 0.15SD [0.02, 0.29] in MR) and with isoleucine in MR analyses (0.22SD [0.08, 0.35]). No consistent evidence was observed for effects of chronotype on metabolomic measures.CONCLUSIONS: Whilst our results suggested that unfavourable sleep traits may not cause widespread metabolic disruption, some notable effects were observed. The evidence for possible effects of insomnia symptoms on glycoprotein acetyls and citrate and longer total sleep duration on creatinine and isoleucine might explain some of the effects, found in MR analyses of these sleep traits on coronary heart disease, which warrant further investigation.</p

    Pathogen and Circadian Controlled 1 (PCC1) Protein Is Anchored to the Plasma Membrane and Interacts with Subunit 5 of COP9 Signalosome in Arabidopsis

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    The Pathogen and Circadian Controlled 1 (PCC1) gene, previously identified and further characterized as involved in defense to pathogens and stress-induced flowering, codes for an 81-amino acid protein with a cysteine-rich C-terminal domain. This domain is essential for homodimerization and anchoring to the plasma membrane. Transgenic plants with the ß- glucuronidase (GUS) reporter gene under the control of 1.1 kb promoter sequence of PCC1 gene display a dual pattern of expression. At early post-germination, PCC1 is expressed only in the root vasculature and in the stomata guard cells of cotyledons. During the transition from vegetative to reproductive development, PCC1 is strongly expressed in the vascular tissue of petioles and basal part of the leaf, and it further spreads to the whole limb in fully expanded leaves. This developmental pattern of expression together with the late flowering phenotype of long-day grown RNA interference (iPCC1) plants with reduced PCC1 expression pointed to a regulatory role of PCC1 in the photoperiod-dependent flowering pathway. iPCC1 plants are defective in light perception and signaling but are not impaired in the function of the core CO-FT module of the photoperiod-dependent pathway. The regulatory effect exerted by PCC1 on the transition to flowering as well as on other reported phenotypes might be explained by a mechanism involving the interaction with the subunit 5 of the COP9 signalosome (CSN).This work was funded by grants BIO2008-00839, BIO2011-27526 and CSD2007-0057 from Ministerio de Ciencia e Innovacion of Spain to J.L. A fellowship/contract of the FPU program of the Ministerio de Educacion y Ciencia (Spain) funded R.M. work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Mir Moreno, R.; Leon Ramos, J. (2014). Pathogen and Circadian Controlled 1 (PCC1) Protein Is Anchored to the Plasma Membrane and Interacts with Subunit 5 of COP9 Signalosome in Arabidopsis. PLoS ONE. 1(9):1-14. https://doi.org/10.1371/journal.pone.0087216S11419Sauerbrunn, N., & Schlaich, N. L. (2004). PCC1 : a merging point for pathogen defence and circadian signalling in Arabidopsis. Planta, 218(4), 552-561. doi:10.1007/s00425-003-1143-zSEGARRA, S., MIR, R., MARTÍNEZ, C., & LEÓN, J. (2009). Genome-wide analyses of the transcriptomes of salicylic acid-deficient versus wild-type plants uncover Pathogen and Circadian Controlled 1 (PCC1) as a regulator of flowering time in Arabidopsis. Plant, Cell & Environment, 33(1), 11-22. doi:10.1111/j.1365-3040.2009.02045.xVenancio, T. M., & Aravind, L. (2009). CYSTM, a novel cysteine-rich transmembrane module with a role in stress tolerance across eukaryotes. Bioinformatics, 26(2), 149-152. doi:10.1093/bioinformatics/btp647Lau, O. S., & Deng, X. W. (2010). Plant hormone signaling lightens up: integrators of light and hormones. Current Opinion in Plant Biology, 13(5), 571-577. doi:10.1016/j.pbi.2010.07.001Seo, M., Nambara, E., Choi, G., & Yamaguchi, S. (2008). Interaction of light and hormone signals in germinating seeds. Plant Molecular Biology, 69(4), 463-472. doi:10.1007/s11103-008-9429-yDe Lucas, M., Davière, J.-M., Rodríguez-Falcón, M., Pontin, M., Iglesias-Pedraz, J. M., Lorrain, S., … Prat, S. (2008). A molecular framework for light and gibberellin control of cell elongation. Nature, 451(7177), 480-484. doi:10.1038/nature06520Feng, S., Martinez, C., Gusmaroli, G., Wang, Y., Zhou, J., Wang, F., … Deng, X. W. (2008). Coordinated regulation of Arabidopsis thaliana development by light and gibberellins. Nature, 451(7177), 475-479. doi:10.1038/nature06448Mutasa-Gottgens, E., & Hedden, P. (2009). Gibberellin as a factor in floral regulatory networks. Journal of Experimental Botany, 60(7), 1979-1989. doi:10.1093/jxb/erp040Bastian, R., Dawe, A., Meier, S., Ludidi, N., Bajic, V. B., & Gehring, C. (2010). Gibberellic acid and cGMP-dependent transcriptional regulation inArabidopsis thaliana. Plant Signaling & Behavior, 5(3), 224-232. doi:10.4161/psb.5.3.10718Yu, S., Galvão, V. C., Zhang, Y.-C., Horrer, D., Zhang, T.-Q., Hao, Y.-H., … Wang, J.-W. (2012). Gibberellin Regulates the Arabidopsis Floral Transition through miR156-Targeted SQUAMOSA PROMOTER BINDING–LIKE Transcription Factors. The Plant Cell, 24(8), 3320-3332. doi:10.1105/tpc.112.101014Arc, E., Galland, M., Cueff, G., Godin, B., Lounifi, I., Job, D., & Rajjou, L. (2011). Reboot the system thanks to protein post-translational modifications and proteome diversity: How quiescent seeds restart their metabolism to prepare seedling establishment. PROTEOMICS, 11(9), 1606-1618. doi:10.1002/pmic.201000641Dill, A., Thomas, S. G., Hu, J., Steber, C. M., & Sun, T. (2004). The Arabidopsis F-Box Protein SLEEPY1 Targets Gibberellin Signaling Repressors for Gibberellin-Induced Degradation. The Plant Cell, 16(6), 1392-1405. doi:10.1105/tpc.020958Wang, F., & Deng, X. W. (2011). Plant ubiquitin-proteasome pathway and its role in gibberellin signaling. Cell Research, 21(9), 1286-1294. doi:10.1038/cr.2011.118Hotton, S. K., & Callis, J. (2008). Regulation of Cullin RING Ligases. Annual Review of Plant Biology, 59(1), 467-489. doi:10.1146/annurev.arplant.58.032806.104011Cope, G. A. (2002). Role of Predicted Metalloprotease Motif of Jab1/Csn5 in Cleavage of Nedd8 from Cul1. Science, 298(5593), 608-611. doi:10.1126/science.1075901Gusmaroli, G., Figueroa, P., Serino, G., & Deng, X. W. (2007). Role of the MPN Subunits in COP9 Signalosome Assembly and Activity, and Their Regulatory Interaction with Arabidopsis Cullin3-Based E3 Ligases. The Plant Cell, 19(2), 564-581. doi:10.1105/tpc.106.047571Serino, G., & Deng, X.-W. (2003). THECOP9 SIGNALOSOME: Regulating Plant Development Through the Control of Proteolysis. Annual Review of Plant Biology, 54(1), 165-182. doi:10.1146/annurev.arplant.54.031902.134847Stratmann, J. W., & Gusmaroli, G. (2012). Many jobs for one good cop – The COP9 signalosome guards development and defense. Plant Science, 185-186, 50-64. doi:10.1016/j.plantsci.2011.10.004Lozano-Juste, J., & León, J. (2011). Nitric Oxide Regulates DELLA Content and PIF Expression to Promote Photomorphogenesis in Arabidopsis. Plant Physiology, 156(3), 1410-1423. doi:10.1104/pp.111.177741Nakagawa, T., Kurose, T., Hino, T., Tanaka, K., Kawamukai, M., Niwa, Y., … Kimura, T. (2007). Development of series of gateway binary vectors, pGWBs, for realizing efficient construction of fusion genes for plant transformation. Journal of Bioscience and Bioengineering, 104(1), 34-41. doi:10.1263/jbb.104.34Fromont-Racine, M., Rain, J.-C., & Legrain, P. (1997). Toward a functional analysis of the yeast genome through exhaustive two-hybrid screens. Nature Genetics, 16(3), 277-282. doi:10.1038/ng0797-277Belda-Palazón B, Ruiz L, Martí E, Tárraga S, Tiburcio AF, et al.. (2012) Aminopropyltransferases involved in polyamine biosynthesis localize preferentially in the nucleus of plant cells. PLoS One 7(10), e46907.Simon, R., Igeño, M. I., & Coupland, G. (1996). Activation of floral meristem identity genes in Arabidopsis. Nature, 384(6604), 59-62. doi:10.1038/384059a0Martínez, C., Pons, E., Prats, G., & León, J. (2003). Salicylic acid regulates flowering time and links defence responses and reproductive development. The Plant Journal, 37(2), 209-217. doi:10.1046/j.1365-313x.2003.01954.xKyte, J., & Doolittle, R. F. (1982). A simple method for displaying the hydropathic character of a protein. Journal of Molecular Biology, 157(1), 105-132. doi:10.1016/0022-2836(82)90515-0Marmagne, A., Rouet, M.-A., Ferro, M., Rolland, N., Alcon, C., Joyard, J., … Ephritikhine, G. (2004). Identification of New Intrinsic Proteins inArabidopsisPlasma Membrane Proteome. Molecular & Cellular Proteomics, 3(7), 675-691. doi:10.1074/mcp.m400001-mcp200Nühse, T. S., Stensballe, A., Jensen, O. N., & Peck, S. C. (2004). Phosphoproteomics of the Arabidopsis Plasma Membrane and a New Phosphorylation Site Database. The Plant Cell, 16(9), 2394-2405. doi:10.1105/tpc.104.023150Kobayashi, Y., & Weigel, D. (2007). Move on up, it’s time for change mobile signals controlling photoperiod-dependent flowering. Genes &amp; Development, 21(19), 2371-2384. doi:10.1101/gad.1589007Jaeger, K. E., & Wigge, P. A. (2007). FT Protein Acts as a Long-Range Signal in Arabidopsis. Current Biology, 17(12), 1050-1054. doi:10.1016/j.cub.2007.05.008Mathieu, J., Warthmann, N., Küttner, F., & Schmid, M. (2007). Export of FT Protein from Phloem Companion Cells Is Sufficient for Floral Induction in Arabidopsis. Current Biology, 17(12), 1055-1060. doi:10.1016/j.cub.2007.05.009Mir, R., Hernández, M. L., Abou-Mansour, E., Martínez-Rivas, J. M., Mauch, F., Métraux, J.-P., & León, J. (2013). Pathogen and Circadian Controlled 1 (PCC1) regulates polar lipid content, ABA-related responses, and pathogen defence in Arabidopsis thaliana. Journal of Experimental Botany, 64(11), 3385-3395. doi:10.1093/jxb/ert177Nordgård, O., Dahle, Ø., Andersen, T. Ø., & Gabrielsen, O. S. (2001). JAB1/CSN5 interacts with the GAL4 DNA binding domain: A note of caution about two-hybrid interactions. Biochimie, 83(10), 969-971. doi:10.1016/s0300-9084(01)01329-3Kwok, S. F., Staub, J. M., & Deng, X.-W. (1999). Characterization of two subunits of Arabidopsis 19S proteasome regulatory complex and its possible interaction with the COP9 complex 1 1Edited by J. Karn. Journal of Molecular Biology, 285(1), 85-95. doi:10.1006/jmbi.1998.2315Nezames, C. D., & Deng, X. W. (2012). The COP9 Signalosome: Its Regulation of Cullin-Based E3 Ubiquitin Ligases and Role in Photomorphogenesis. Plant Physiology, 160(1), 38-46. doi:10.1104/pp.112.198879Moon, J., Parry, G., & Estelle, M. (2004). The Ubiquitin-Proteasome Pathway and Plant Development. The Plant Cell, 16(12), 3181-3195. doi:10.1105/tpc.104.161220Dreher, K., & Callis, J. (2007). Ubiquitin, Hormones and Biotic Stress in Plants. Annals of Botany, 99(5), 787-822. doi:10.1093/aob/mcl255Parry, G., & Estelle, M. (2004). Regulation of cullin-based ubiquitin ligases by the Nedd8/RUB ubiquitin-like proteins. Seminars in Cell & Developmental Biology, 15(2), 221-229. doi:10.1016/j.semcdb.2003.12.003Wee, S., Geyer, R. K., Toda, T., & Wolf, D. A. (2005). CSN facilitates Cullin–RING ubiquitin ligase function by counteracting autocatalytic adapter instability. Nature Cell Biology, 7(4), 387-391. doi:10.1038/ncb1241Kuramata, M., Masuya, S., Takahashi, Y., Kitagawa, E., Inoue, C., Ishikawa, S., … Kusano, T. (2008). Novel Cysteine-Rich Peptides from Digitaria ciliaris and Oryza sativa Enhance Tolerance to Cadmium by Limiting its Cellular Accumulation. Plant and Cell Physiology, 50(1), 106-117. doi:10.1093/pcp/pcn175Zeng, W., Melotto, M., & He, S. Y. (2010). Plant stomata: a checkpoint of host immunity and pathogen virulence. Current Opinion in Biotechnology, 21(5), 599-603. doi:10.1016/j.copbio.2010.05.006Wigge, P. A. (2011). FT, A Mobile Developmental Signal in Plants. Current Biology, 21(9), R374-R378. doi:10.1016/j.cub.2011.03.038Kardailsky, I. (1999). Activation Tagging of the Floral Inducer FT. Science, 286(5446), 1962-1965. doi:10.1126/science.286.5446.1962Srikanth, A., & Schmid, M. (2011). Regulation of flowering time: all roads lead to Rome. Cellular and Molecular Life Sciences, 68(12), 2013-2037. doi:10.1007/s00018-011-0673-yGalvao, V. C., Horrer, D., Kuttner, F., & Schmid, M. (2012). Spatial control of flowering by DELLA proteins in Arabidopsis thaliana. Development, 139(21), 4072-4082. doi:10.1242/dev.080879Cerdán, P. D., & Chory, J. (2003). Regulation of flowering time by light quality. Nature, 423(6942), 881-885. doi:10.1038/nature01636Guo, H. (1998). Regulation of Flowering Time by Arabidopsis Photoreceptors. Science, 279(5355), 1360-1363. doi:10.1126/science.279.5355.1360Liu, B., Zuo, Z., Liu, H., Liu, X., & Lin, C. (2011). Arabidopsis cryptochrome 1 interacts with SPA1 to suppress COP1 activity in response to blue light. Genes & Development, 25(10), 1029-1034. doi:10.1101/gad.2025011Weidler, G., zur Oven-Krockhaus, S., Heunemann, M., Orth, C., Schleifenbaum, F., Harter, K., … Batschauer, A. (2012). Degradation of Arabidopsis CRY2 Is Regulated by SPA Proteins and Phytochrome A. The Plant Cell, 24(6), 2610-2623. doi:10.1105/tpc.112.09821

    Nitric oxide triggers a transient metabolic reprogramming in Arabidopsis

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    [EN] Nitric oxide (NO) regulates plant growth and development as well as responses to stress that enhanced its endogenous production. Arabidopsis plants exposed to a pulse of exogenous NO gas were used for untargeted global metabolomic analyses thus allowing the identification of metabolic processes affected by NO. At early time points after treatment, NO scavenged superoxide anion and induced the nitration and the S-nitrosylation of proteins. These events preceded an extensive though transient metabolic reprogramming at 6&#8201;h after NO treatment, which included enhanced levels of polyamines, lipid catabolism and accumulation of phospholipids, chlorophyll breakdown, protein and nucleic acid turnover and increased content of sugars. Accordingly, lipid-related structures such as root cell membranes and leaf cuticle altered their permeability upon NO treatment. Besides, NO-treated plants displayed degradation of starch granules, which is consistent with the increased sugar content observed in the metabolomic survey. The metabolic profile was restored to baseline levels at 24&#8201;h post-treatment, thus pointing up the plasticity of plant metabolism in response to nitroxidative stress conditions.This work was supported by grants BIO2011-27526 and BIO2014-56067-P from the Spanish Ministry of Economy and Competitiveness and FEDER funds. We thank support and comments from Danny Alexander (Metabolon Inc., USA) on metabolomic analyses.Leon Ramos, J.; Costa-Broseta, Á.; Castillo López Del Toro, MC. (2016). Nitric oxide triggers a transient metabolic reprogramming in Arabidopsis. Scientific Reports. 6:1-14. doi:10.1038/srep37945S1146Arc, E., Galland, M., Godin, B., Cueff, G. & Rajjou, L. Nitric oxide implication in the control of seed dormancy and germination. Front. Plant Sci. 4, 346 (2013).Beligni, M. V. & Lamattina, L. Nitric oxide stimulates seed germination and de-etiolation, and inhibits hypocotyl elongation, three light-inducible responses in plants. Planta 210, 215–221 (2000).Lozano-Juste, J. & León, J. Nitric oxide regulates DELLA content and PIF expression to promote photomorphogenesis in Arabidopsis. Plant Physiol. 156, 1410–1123 (2011).He, Y. et al. Nitric oxide represses the Arabidopsis floral transition. Science 305, 1968–1971 (2004).Tsai, Y. C., Delk, N. A., Chowdhury, N. I. & Braam, J. Arabidopsis potential calcium sensors regulate nitric oxide levels and the transition to flowering. Plant Signal. Behav. 2, 446–454 (2007).Manjunatha, G., Lokesh, V. & Neelwarne, B. Nitric oxide in fruit ripening: trends and opportunities. Biotechnol. Adv. 28, 489–499 (2010).Liu, F. & Guo, F. Q. Nitric oxide deficiency accelerates chlorophyll breakdown and stability loss of thylakoid membranes during dark-induced leaf senescence in Arabidopsis. PLoS One 8(2), e56345 (2013).Du, J. et al. Nitric oxide induces cotyledon senescence involving co-operation of the NES1/MAD1 and EIN2-associated ORE1 signalling pathways in Arabidopsis. J. Exp. Bot. 65, 4051–4063 (2014).Siddiqui, M. H., Al-Whaibi, M. H. & Basalah, M. O. Role of nitric oxide in tolerance of plants to abiotic stress. Protoplasma 248, 447–455 (2011).Arasimowicz-Jelonek, M. & Floryszak-Wieczorek, J. Nitric oxide: an effective weapon of the plant or the pathogen? Mol. Plant Pathol. 15, 406–416 (2014).Thomas, D. D. Breathing new life into nitric oxide signaling: A brief overview of the interplay between oxygen and nitric oxide. Redox Biol. 5, 225–33 (2015).Groβ, F., Durner, J. & Gaupels, F. Nitric oxide, antioxidants and prooxidants in plant defence responses. Front. Plant Sci. 4, 419 (2013).Astier, J. & Lindermayr, C. Nitric oxide-dependent posttranslational modification in plants: an update. Int. J. Mol. Sci. 13, 15193–15208 (2012).Hess, D. T. & Stamler, J. S. Regulation by S-nitrosylation of protein post-translational modification. J. Biol. Chem. 287, 4411–4418 (2012).Guerra, D. D. & Callis, J. Ubiquitin on the move: the ubiquitin modification system plays diverse roles in the regulation of endoplasmic reticulum- and plasma membrane-localized proteins. Plant Physiol. 160, 56–64 (2012).Skalska, K., Miller, J. S. & Ledakowicz, S. Trends in NO(x) abatement: a review. Sci. Total Environ. 408, 3976–3989 (2010).Pilegaard, K. Processes regulating nitric oxide emissions from soils. Phil. Transac. Royal Soc. London. Ser. B, Biol. Sci. 368, 20130126 (2013).Jaegle, L., Steinberger, L., Martin, R. V. & Chance, K. Global partitioning of NOx sources using satellite observations: Relative roles of fossil fuel combustion, biomass burning and soil emissions. Faraday Discus. 130, 407–423 (2005).Gupta, K. J., Fernie, A. R., Kaiser, W. M. & van Dongen, J. T. On the origins of nitric oxide. Trends Plant Sci. 16, 160–168 (2011).Mur, L. A. et al. Nitric oxide in plants: an assessment of the current state of knowledge. AoB Plants 5, pls052 (2013).Correa-Aragunde, N., Foresi, N. & Lamattina, L. Nitric oxide is a ubiquitous signal for maintaining redox balance in plant cells: regulation of ascorbate peroxidase as a case study. J. Exp. Bot. 66, 2913–2921 (2015).Noctor, G., Lelarge-Trouverie, C. & Mhamdi, A. The metabolomics of oxidative stress. Phytochemistry 112, 33–53 (2015).Allan, W. L., Simpson, J. P., Clark, S. M. & Shelp, B. J. Gamma-hydroxybutyrate accumulation in Arabidopsis and tobacco plants is a general response to abiotic stress: putative regulation by redox balance and glyoxylate reductase isoforms. J. Exp. Bot. 59, 2555–2564 (2008).Romero, L. C., Aroca, M. Á., Laureano-Marín, A. M., Moreno, I., García, I. & Gotor, C. Cysteine and cysteine-related signaling pathways in Arabidopsis thaliana. Mol. Plant 7, 264–276 (2014).Noctor, G. et al. Glutathione in plants: an integrated overview. Plant Cell Environ. 35, 454–484 (2012).Feussner, I. & Wasternack, C. The lipoxygenase pathway. Ann. Rev. Plant Biol. 53, 275–297 (2002).Green, M. A. & Fry, S. C. Vitamin C degradation in plant cells via enzymatic hydrolysis of 4-O-oxalyl-L-threonate. Nature 433, 83–87 (2005).Szarka, A., Tomasskovics, B. & Bánhegyi, G. The ascorbate-glutathione-α-tocopherol triad in abiotic stress response. Int. J. Mol. Sci. 13, 4458–4483 (2012).Hurlock, A. K., Roston, R. L., Wang, K. & Benning, C. Lipid trafficking in plant cells. Traffic 15, 915–932 (2014).Blokhina, O., Virolainen, E. & Fagerstedt, K. V. Antioxidants, oxidative damage and oxygen deprivation stress: a review. Ann. Bot. 91, 179–194 (2003).Yeats, T. H. & Rose, J. K. The formation and function of plant cuticles. Plant Physiol. 163, 5–20 (2013).Lozano-Juste, J. & León, J. Enhanced abscisic acid-mediated responses in nia1nia2noa1-2 triple mutant impaired in NIA/NR- and AtNOA1-dependent nitric oxide biosynthesis in Arabidopsis. Plant Physiol. 152, 891–903 (2010).Hörtensteiner, S. Update on the biochemistry of chlorophyll breakdown. Plant Mol Biol. 82, 505–17 (2013).Pruzinská, A. et al. Chlorophyll breakdown in senescent Arabidopsis leaves: characterization of chlorophyll catabolites and of chlorophyll catabolic enzymes involved in the degreening reaction. Plant Physiol. 139, 52–63 (2005).Hirashima, M., Tanaka, R. & Tanaka, A. Light-independent cell death induced by accumulation of pheophorbide a in Arabidopsis thaliana. Plant Cell Physiol. 50, 719–29 (2009).Zottini, M., Costa, A., De Michele, R., Ruzzene, M., Carimi, F. & Lo Schiavo, F. Salicylic acid activates nitric oxide synthesis in Arabidopsis. J Exp Bot. 58, 1397–1405 (2007).Mainz, E. R. et al. Monitoring intracellular nitric oxide production using microchip electrophoresis and laser-induced fluorescence detection. Analytical Methods 4, 414–420 (2012).Vandelle, E. & Delledonne, M. Peroxynitrite formation and function in plants. Plant Sci. 181, 534–539 (2011).Minocha, R., Majumdar, R. & Minocha, S. C. Polyamines and abiotic stress in plants: a complex relationship. Front. Plant Sci. 5, 175 (2014).Parsons H. T., Yasmin, T. & Fry, S. C. Alternative pathways of dehydroascorbic acid degradation in vitro and in plant cell cultures: novel insights into vitamin C catabolism. Biochem. J. 440, 375–383 (2011).Hou, Q., Ufer, G. & Bartels, D. Lipid signalling in plant responses to abiotic stress. Plant Cell Environ. 39, 1029–4108 (2016).Zhou, X. R., Callahan, D. L., Shrestha, P., Liu, Q., Petrie, J. R. & Singh, S. P. Lipidomic analysis of Arabidopsis seed genetically engineered to contain DHA. Front. Plant Sci. 5, 41 (2014).Pohl, C. H. & Kock, J. L. Oxidized fatty acids as inter-kingdom signaling molecules. Molecules 19, 1273–1285 (2014).Araújo, W. L., Tohge, T., Ishizaki, K., Leaver, C. J. & Fernie, A. R. Protein degradation-an alternative respiratory substrate for stressed plants. Trends Plant Sci. 16, 489–498 (2011).Sakamoto, W. & Takami, T. Nucleases in higher plants and their possible involvement in DNA degradation during leaf senescence. J. Exp. Bot. 65, 3835–3843 (2014).Del Duca, S., Serafini-Fracassini, D. & Cai, G. Senescence and programmed cell death in plants: polyamine action mediated by transglutaminase. Front. Plant Sci. 5, 120 (2014).Franco, M. C. & Estévez, A. G. Tyrosine nitration as mediator of cell death. Cell. Mol. Life Sci. 71, 3939–3950 (2014).Palumbo, A., Fiore, G., Di Cristo, C., Di Cosmo, A. & d’Ischia, M. NMDA receptor stimulation induces temporary alpha-tubulin degradation signalled by nitric oxide-mediated tyrosine nitration in the nervous system of Sepia officinalis. Biochem. Biophys. Res. Commun. 293, 1536–1543 (2002).Wang, Y. Y., Lin, S. Y., Chuang, Y. H., Mao, C. H., Tung, K. C. & Sheu, W. H. Protein nitration is associated with increased proteolysis in skeletal muscle of bile duct ligation-induced cirrhotic rats. Metabolism 59, 468–472 (2010).Castillo, M. C., Lozano-Juste, J., González-Guzmán, M., Rodriguez, L., Rodriguez, P. L. & León, J. Inactivation of PYR/PYL/RCAR ABA receptors by tyrosine nitration may enable rapid inhibition of ABA signaling by nitric oxide in plants. Sci. Signal. 8(392), ra89 (2015).Blaise, G. A., Gauvin, D., Gangal, M. & Authier, S. Nitric oxide, cell signaling and cell death. Toxicology 208, 177–192 (2005).Brüne, B. Nitric oxide: NO apoptosis or turning it ON? Cell Death Differ. 10, 864–869 (2003).Wang, Y., Chen, C., Loake, G. J. & Chu, C. Nitric oxide: promoter or suppressor of programmed cell death? Prot. Cell 1, 133–142 (2010).Serrano, I., Romero-Puertas, M. C., Sandalio, L. M. & Olmedilla, A. The role of reactive oxygen species and nitric oxide in programmed cell death associated with self-incompatibility. J. Exp. Bot. 66, 2869–2876 (2015).Huang, S., Hill, R. D. & Stasolla, C. Plant hemoglobin participation in cell fate determination. Plant Signal. Behavior 9, e29485 (2014).Maes, M. B., Scharpé, S. & De Meester, I. Dipeptidyl peptidase II (DPPII), a review. Clin. Chim. Acta 380, 31–49 (2007).Gibbs, D. J. et al. Nitric oxide sensing in plants is mediated by proteolytic control of group VII ERF transcription factors. Mol. Cell 53, 369–379 (2014).Kitamura, K. Inhibition of the Arg/N-end rule pathway-mediated proteolysis by dipeptide-mimetic molecules. Amino Acids 48, 235–243 (2016).Duek, P. D., Elmer, M. V., van Oosten, V. R. & Fankhauser C. The degradation of HFR1, a putative bHLH class transcription factor involved in light signaling, is regulated by phosphorylation and requires COP1. Curr Biol. 14, 2296–2301 (2004)

    End-bridging monte carlo simulation of bulk and grafted amorphous polyethylene above and below the glass transition

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    The very efficient end-bridging Monte Carlo (EBMC) method has been employed in order to simulate an amorphous, polydisperse 80-chain large C156 polyethylene (PE) system in atomistic detail over a wide range of temperatures (from 600 down to 150 K) and determine its glass transition temperature (Tg). Two sets of simulations have been performed: one with a bulk, isotropic sample and the other with a thin film in which all the 80 PE chains were grafted on a hard substrate on one side (corresponding to a high grafting density equal to = 1.75 nm-2) and exposed to vacuum on the other side. In the simulations, a united-atom model was employed for PE ensuring that only the purely amorphous phase of PE was simulated at all temperatures. In all cases, very long simulations were carried out in order to give enough time for the system to relax at all length scales. For all temperatures studied, the longest relaxation time was found to be present by descriptors associated with the system's long-range conformational characteristics. In contrast, more local, internal structural features were always faster in equilibrating. As a result, the time autocorrelation function for the chain end-to-end unit vector, fu(t), was found to drop to zero and then clearly fluctuate around this value only for temperatures higher than about 220 K for both systems. For lower temperatures, fu(t) did not relax completely, even after 2 × 107 CPU seconds. Additional volumetric simulation data demonstrated a sharp change in the density and potential energy of both systems in the neighborhood of the 230 K, which are considered as features of the glass transition for amorphous PE. The Tg value suggested by the present EBMC simulations for amorphous (bulk or grafted) PE is (230 ± 10) K, which is consistent with the value of 237 K measured experimentally by Wunderlich [J. of Chem. Phys. 1962, 37, 1203] and Loufakis and Wunderlich [J. Phys. Chem. 1988, 92, 4205] for PE in the limit of zero crystallinity. Further, the predicted change in the heat capacity at constant pressure at the glass transition is cp = 1.2 × 10-4 kcal g-1 K-1, which is very close to the value of 1.5 × 10-4 kcal g-1 K-1 measured experimentally by Wunderlich [J. of Chem. Phys. 1962, 37, 1203]. Additional results on the temperature dependence of the conformational and structural properties in the two PE systems are also reported and discussed in detail. -------------------------------------------------------------------------------
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