160 research outputs found
Isolation and fine mapping of Rps6: An intermediate host resistance gene in barley to wheat stripe rust
A plant may be considered a nonhost of a pathogen if all known genotypes of a plant species are resistant to all known isolates of a pathogen species. However, if a small number of genotypes are susceptible to some known isolates of a pathogen species this plant maybe considered an intermediate host. Barley (Hordeum vulgare) is an intermediate host for Puccinia striiformis f. sp. tritici (Pst), the causal agent of wheat stripe rust. We wanted to understand the genetic architecture underlying resistance to Pst and to determine whether any overlap exists with resistance to the host pathogen, Puccinia striiformis f. sp. hordei (Psh). We mapped Pst resistance to chromosome 7H and show that host and intermediate host resistance is genetically uncoupled. Therefore, we designate this resistance locus Rps6. We used phenotypic and genotypic selection on F2:3 families to isolate Rps6 and fine mapped the locus to a 0.1 cM region. Anchoring of the Rps6 locus to the barley physical map placed the region on two adjacent fingerprinted contigs. Efforts are now underway to sequence the minimal tiling path and to delimit the physical region harbouring Rps6. This will facilitate additional marker development and permit identification of candidate genes in the region
Distribution of causes of maternal mortality among different socio-demographic groups in Ghana; a descriptive study
BACKGROUND: Ghana's maternal mortality ratio remains high despite efforts made to meet Millennium Development Goal 5. A number of studies have been conducted on maternal mortality in Ghana; however, little is known about how the causes of maternal mortality are distributed in different socio-demographic subgroups. Therefore the aim of this study was to assess and analyse the causes of maternal mortality according to socio-demographic factors in Ghana.METHODS: The causes of maternal deaths were assessed with respect to age, educational level, rural/urban residence status and marital status. Data from a five year retrospective survey was used. The data was obtained from Ghana Maternal Health Survey 2007 acquired from the database of Ghana Statistical Service. A total of 605 maternal deaths within the age group 12-49 years were analysed using frequency tables, cross-tabulations and logistic regression.RESULTS: Haemorrhage was the highest cause of maternal mortality (22.8%). Married women had a significantly higher risk of dying from haemorrhage, compared with single women (adjusted OR = 2.7, 95%CI = 1.2-5.7). On the contrary, married women showed a significantly reduced risk of dying from abortion compared to single women (adjusted OR = 0.2, 95%CI = 0.1-0.4). Women aged 35-39 years had a significantly higher risk of dying from haemorrhage (aOR 2.6, 95%CI = 1.4-4.9), whereas they were at a lower risk of dying from abortion (aOR 0.3, 95% CI = 0.1-0.7) compared to their younger counterparts. The risk of maternal death from infectious diseases decreased with increasing maternal age, whereas the risk of dying from miscellaneous causes increased with increasing age.CONCLUSIONS: The study shows evidence of variations in the causes of maternal mortality among different socio-demographic subgroups in Ghana that should not be overlooked. It is therefore recommended that interventions aimed at combating the high maternal mortality in Ghana should be both cause-specific as well as target-specific
An Automated Recording Method in Clinical Consultation to Rate the Limp in Lower Limb Osteoarthritis
For diagnosis and follow up, it is important to be able to quantify limp in an objective, and precise way adapted to daily clinical consultation. The purpose of this exploratory study was to determine if an inertial sensor-based method could provide simple features that correlate with the severity of lower limb osteoarthritis evaluated by the WOMAC index without the use of step detection in the signal processing. Forty-eight patients with lower limb osteoarthritis formed two severity groups separated by the median of the WOMAC index (G1, G2). Twelve asymptomatic age-matched control subjects formed the control group (G0). Subjects were asked to walk straight 10 meters forward and 10 meters back at self-selected walking speeds with inertial measurement units (IMU) (3-D accelerometers, 3-D gyroscopes and 3-D magnetometers) attached on the head, the lower back (L3-L4) and both feet. Sixty parameters corresponding to the mean and the root mean square (RMS) of the recorded signals on the various sensors (head, lower back and feet), in the various axes, in the various frames were computed. Parameters were defined as discriminating when they showed statistical differences between the three groups. In total, four parameters were found discriminating: mean and RMS of the norm of the acceleration in the horizontal plane for contralateral and ipsilateral foot in the doctor’s office frame. No discriminating parameter was found on the head or the lower back. No discriminating parameter was found in the sensor linked frames. This study showed that two IMUs placed on both feet and a step detection free signal processing method could be an objective and quantitative complement to the clinical examination of the physician in everyday practice. Our method provides new automatically computed parameters that could be used for the comprehension of lower limb osteoarthritis. It may not only be used in medical consultation to score patients but also to monitor the evolution of their clinical syndrome during and after rehabilitation. Finally, it paves the way for the quantification of gait in other fields such as neurology and for monitoring the gait at a patient’s home
Genomic Fossils Calibrate the Long-Term Evolution of Hepadnaviruses
Ancient hepadnavirus sequences found in bird genomes reveal that this family of viruses, which includes the human hepatitis B virus, is much older than previously thought
Glacial Refugia in Pathogens: European Genetic Structure of Anther Smut Pathogens on Silene latifolia and Silene dioica
Climate warming is predicted to increase the frequency of invasions by pathogens and to cause the large-scale redistribution of native host species, with dramatic consequences on the health of domesticated and wild populations of plants and animals. The study of historic range shifts in response to climate change, such as during interglacial cycles, can help in the prediction of the routes and dynamics of infectious diseases during the impending ecosystem changes. Here we studied the population structure in Europe of two Microbotryum species causing anther smut disease on the plants Silene latifolia and Silene dioica. Clustering analyses revealed the existence of genetically distinct groups for the pathogen on S. latifolia, providing a clear-cut example of European phylogeography reflecting recolonization from southern refugia after glaciation. The pathogen genetic structure was congruent with the genetic structure of its host species S. latifolia, suggesting dependence of the migration pathway of the anther smut fungus on its host. The fungus, however, appeared to have persisted in more numerous and smaller refugia than its host and to have experienced fewer events of large-scale dispersal. The anther smut pathogen on S. dioica also showed a strong phylogeographic structure that might be related to more northern glacial refugia. Differences in host ecology probably played a role in these differences in the pathogen population structure. Very high selfing rates were inferred in both fungal species, explaining the low levels of admixture between the genetic clusters. The systems studied here indicate that migration patterns caused by climate change can be expected to include pathogen invasions that follow the redistribution of their host species at continental scales, but also that the recolonization by pathogens is not simply a mirror of their hosts, even for obligate biotrophs, and that the ecology of hosts and pathogen mating systems likely affects recolonization patterns
A meta-analysis reveals the commonalities and differences in Arabidopsis thaliana response to different viral pathogens
Understanding the mechanisms by which plants trigger host defenses in response to viruses has been a challenging problem owing to the multiplicity of factors and complexity of interactions involved. The advent of genomic techniques, however, has opened the possibility to grasp a global picture of the interaction. Here, we used Arabidopsis thaliana to identify and compare genes that are differentially regulated upon infection with seven distinct (+)ssRNA and one ssDNA plant viruses. In the first approach, we established lists of genes differentially affected by each virus and compared their involvement in biological functions and metabolic processes. We found that phylogenetically related viruses significantly alter the expression of similar genes and that viruses naturally infecting Brassicaceae display a greater overlap in the plant response. In the second approach, virus-regulated genes were contextualized using models of transcriptional and protein-protein interaction networks of A. thaliana. Our results confirm that host cells undergo significant reprogramming of their transcriptome during infection, which is possibly a central requirement for the mounting of host defenses. We uncovered a general mode of action in which perturbations preferentially affect genes that are highly connected, central and organized in modules. © 2012 Rodrigo et al.This work was supported by the Spanish Ministerio de Ciencia e Innovacion (MICINN) grants BFU2009-06993 (S. F. E.) and BIO2006-13107 (C. L.) and by Generalitat Valenciana grant PROMETEO2010/016 (S. F. E.). G. R. is supported by a graduate fellowship from the Generalitat Valenciana (BFPI2007-160) and J.C. by a contract from MICINN grant TIN2006-12860. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Rodrigo Tarrega, G.; Carrera Montesinos, J.; Ruiz-Ferrer, V.; Del Toro, F.; Llave, C.; Voinnet, O.; Elena Fito, SF. (2012). A meta-analysis reveals the commonalities and differences in Arabidopsis thaliana response to different viral pathogens. PLoS ONE. 7(7):40526-40526. https://doi.org/10.1371/journal.pone.0040526S405264052677Peng, X., Chan, E. Y., Li, Y., Diamond, D. L., Korth, M. J., & Katze, M. G. (2009). Virus–host interactions: from systems biology to translational research. Current Opinion in Microbiology, 12(4), 432-438. doi:10.1016/j.mib.2009.06.003Dodds, P. N., & Rathjen, J. P. (2010). Plant immunity: towards an integrated view of plant–pathogen interactions. Nature Reviews Genetics, 11(8), 539-548. doi:10.1038/nrg2812Maule, A., Leh, V., & Lederer, C. (2002). The dialogue between viruses and hosts in compatible interactions. Current Opinion in Plant Biology, 5(4), 279-284. doi:10.1016/s1369-5266(02)00272-8Whitham, S. A., Quan, S., Chang, H.-S., Cooper, B., Estes, B., Zhu, T., … Hou, Y.-M. (2003). Diverse RNA viruses elicit the expression of common sets of genes in susceptibleArabidopsis thalianaplants. The Plant Journal, 33(2), 271-283. doi:10.1046/j.1365-313x.2003.01625.xBailer, S., & Haas, J. (2009). Connecting viral with cellular interactomes. Current Opinion in Microbiology, 12(4), 453-459. doi:10.1016/j.mib.2009.06.004Whitham, S. A., Yang, C., & Goodin, M. M. (2006). Global Impact: Elucidating Plant Responses to Viral Infection. Molecular Plant-Microbe Interactions, 19(11), 1207-1215. doi:10.1094/mpmi-19-1207MacPherson, J. I., Dickerson, J. E., Pinney, J. W., & Robertson, D. L. (2010). Patterns of HIV-1 Protein Interaction Identify Perturbed Host-Cellular Subsystems. PLoS Computational Biology, 6(7), e1000863. doi:10.1371/journal.pcbi.1000863Jenner, R. G., & Young, R. A. (2005). Insights into host responses against pathogens from transcriptional profiling. Nature Reviews Microbiology, 3(4), 281-294. doi:10.1038/nrmicro1126Andeweg, A. C., Haagmans, B. L., & Osterhaus, A. D. (2008). Virogenomics: the virus–host interaction revisited. Current Opinion in Microbiology, 11(5), 461-466. doi:10.1016/j.mib.2008.09.010Elena, S. F., Carrera, J., & Rodrigo, G. (2011). A systems biology approach to the evolution of plant–virus interactions. Current Opinion in Plant Biology, 14(4), 372-377. doi:10.1016/j.pbi.2011.03.013Tan, S.-L., Ganji, G., Paeper, B., Proll, S., & Katze, M. G. (2007). Systems biology and the host response to viral infection. Nature Biotechnology, 25(12), 1383-1389. doi:10.1038/nbt1207-1383De la Fuente, A. (2010). From ‘differential expression’ to ‘differential networking’ – identification of dysfunctional regulatory networks in diseases. Trends in Genetics, 26(7), 326-333. doi:10.1016/j.tig.2010.05.001Albert, R. (2005). Scale-free networks in cell biology. Journal of Cell Science, 118(21), 4947-4957. doi:10.1242/jcs.02714Yu, H., Braun, P., Yildirim, M. A., Lemmens, I., Venkatesan, K., Sahalie, J., … Vidal, M. (2008). High-Quality Binary Protein Interaction Map of the Yeast Interactome Network. Science, 322(5898), 104-110. doi:10.1126/science.1158684Barabási, A.-L., & Oltvai, Z. N. (2004). Network biology: understanding the cell’s functional organization. Nature Reviews Genetics, 5(2), 101-113. doi:10.1038/nrg1272Albert, R., Jeong, H., & Barabási, A.-L. (2000). Error and attack tolerance of complex networks. Nature, 406(6794), 378-382. doi:10.1038/35019019Mukhtar, M. S., Carvunis, A.-R., Dreze, M., Epple, P., Steinbrenner, J., … Moore, J. (2011). Independently Evolved Virulence Effectors Converge onto Hubs in a Plant Immune System Network. Science, 333(6042), 596-601. doi:10.1126/science.1203659Calderwood, M. A., Venkatesan, K., Xing, L., Chase, M. R., Vazquez, A., Holthaus, A. M., … Johannsen, E. (2007). Epstein-Barr virus and virus human protein interaction maps. Proceedings of the National Academy of Sciences, 104(18), 7606-7611. doi:10.1073/pnas.0702332104De Chassey, B., Navratil, V., Tafforeau, L., Hiet, M. S., Aublin‐Gex, A., Agaugué, S., … Lotteau, V. (2008). Hepatitis C virus infection protein network. Molecular Systems Biology, 4(1), 230. doi:10.1038/msb.2008.66Shapira, S. D., Gat-Viks, I., Shum, B. O. V., Dricot, A., de Grace, M. M., Wu, L., … Hacohen, N. (2009). A Physical and Regulatory Map of Host-Influenza Interactions Reveals Pathways in H1N1 Infection. Cell, 139(7), 1255-1267. doi:10.1016/j.cell.2009.12.018Dyer, M. D., Murali, T. M., & Sobral, B. W. (2008). The Landscape of Human Proteins Interacting with Viruses and Other Pathogens. PLoS Pathogens, 4(2), e32. doi:10.1371/journal.ppat.0040032Golem, S., & Culver, J. N. (2003). Tobacco mosaic virusInduced Alterations in the Gene Expression Profile ofArabidopsis thaliana. Molecular Plant-Microbe Interactions, 16(8), 681-688. doi:10.1094/mpmi.2003.16.8.681Espinoza, C., Medina, C., Somerville, S., & Arce-Johnson, P. (2007). Senescence-associated genes induced during compatible viral interactions with grapevine and Arabidopsis. Journal of Experimental Botany, 58(12), 3197-3212. doi:10.1093/jxb/erm165Yang, C., Guo, R., Jie, F., Nettleton, D., Peng, J., Carr, T., … Whitham, S. A. (2007). Spatial Analysis ofArabidopsis thalianaGene Expression in Response toTurnip mosaic virusInfection. Molecular Plant-Microbe Interactions, 20(4), 358-370. doi:10.1094/mpmi-20-4-0358Agudelo-Romero, P., Carbonell, P., de la Iglesia, F., Carrera, J., Rodrigo, G., Jaramillo, A., … Elena, S. F. (2008). Changes in the gene expression profile of Arabidopsis thaliana after infection with Tobacco etch virus. Virology Journal, 5(1), 92. doi:10.1186/1743-422x-5-92Agudelo-Romero, P., Carbonell, P., Perez-Amador, M. A., & Elena, S. F. (2008). Virus Adaptation by Manipulation of Host’s Gene Expression. PLoS ONE, 3(6), e2397. doi:10.1371/journal.pone.0002397Ascencio-Ibáñez, J. T., Sozzani, R., Lee, T.-J., Chu, T.-M., Wolfinger, R. D., Cella, R., & Hanley-Bowdoin, L. (2008). Global Analysis of Arabidopsis Gene Expression Uncovers a Complex Array of Changes Impacting Pathogen Response and Cell Cycle during Geminivirus Infection. Plant Physiology, 148(1), 436-454. doi:10.1104/pp.108.121038Babu, M., Griffiths, J. S., Huang, T.-S., & Wang, A. (2008). Altered gene expression changes in Arabidopsis leaf tissues and protoplasts in response to Plum pox virus infection. BMC Genomics, 9(1), 325. doi:10.1186/1471-2164-9-325De Vienne, D. M., Giraud, T., & Martin, O. C. (2007). A congruence index for testing topological similarity between trees. Bioinformatics, 23(23), 3119-3124. doi:10.1093/bioinformatics/btm500Wise, R. P., Moscou, M. J., Bogdanove, A. J., & Whitham, S. A. (2007). Transcript Profiling in Host–Pathogen Interactions. Annual Review of Phytopathology, 45(1), 329-369. doi:10.1146/annurev.phyto.45.011107.143944Handford, M. G., & Carr, J. P. (2007). A defect in carbohydrate metabolism ameliorates symptom severity in virus-infected Arabidopsis thaliana. Journal of General Virology, 88(1), 337-341. doi:10.1099/vir.0.82376-0Hou, B., Lim, E.-K., Higgins, G. S., & Bowles, D. J. (2004). N-Glucosylation of Cytokinins by Glycosyltransferases ofArabidopsis thaliana. Journal of Biological Chemistry, 279(46), 47822-47832. doi:10.1074/jbc.m409569200Schwender, J., Goffman, F., Ohlrogge, J. B., & Shachar-Hill, Y. (2004). Rubisco without the Calvin cycle improves the carbon efficiency of developing green seeds. Nature, 432(7018), 779-782. doi:10.1038/nature03145Pagán, I., Alonso-Blanco, C., & García-Arenal, F. (2008). Host Responses in Life-History Traits and Tolerance to Virus Infection in Arabidopsis thaliana. PLoS Pathogens, 4(8), e1000124. doi:10.1371/journal.ppat.1000124Carrera, J., Rodrigo, G., Jaramillo, A., & Elena, S. F. (2009). Reverse-engineering the Arabidopsis thaliana transcriptional network under changing environmental conditions. Genome Biology, 10(9), R96. doi:10.1186/gb-2009-10-9-r96Geisler-Lee, J., O’Toole, N., Ammar, R., Provart, N. J., Millar, A. H., & Geisler, M. (2007). A Predicted Interactome for Arabidopsis. Plant Physiology, 145(2), 317-329. doi:10.1104/pp.107.103465Ma, S., Gong, Q., & Bohnert, H. J. (2007). An Arabidopsis gene network based on the graphical Gaussian model. Genome Research, 17(11), 1614-1625. doi:10.1101/gr.6911207Yamada, T., & Bork, P. (2009). Evolution of biomolecular networks — lessons from metabolic and protein interactions. Nature Reviews Molecular Cell Biology, 10(11), 791-803. doi:10.1038/nrm2787Humphries, M. D., & Gurney, K. (2008). Network ‘Small-World-Ness’: A Quantitative Method for Determining Canonical Network Equivalence. PLoS ONE, 3(4), e0002051. doi:10.1371/journal.pone.0002051Stumpf, M. P. H., & Ingram, P. J. (2005). Probability models for degree distributions of protein interaction networks. Europhysics Letters (EPL), 71(1), 152-158. doi:10.1209/epl/i2004-10531-8Khanin, R., & Wit, E. (2006). How Scale-Free Are Biological Networks. Journal of Computational Biology, 13(3), 810-818. doi:10.1089/cmb.2006.13.810Daudin, J.-J., Picard, F., & Robin, S. (2007). A mixture model for random graphs. Statistics and Computing, 18(2), 173-183. doi:10.1007/s11222-007-9046-7Uetz, P. (2006). Herpesviral Protein Networks and Their Interaction with the Human Proteome. Science, 311(5758), 239-242. doi:10.1126/science.1116804Choi, I.-R., Stenger, D. C., & French, R. (2000). Multiple Interactions among Proteins Encoded by the Mite-Transmitted Wheat Streak Mosaic Tritimovirus. Virology, 267(2), 185-198. doi:10.1006/viro.1999.0117Guo, D., Saarma, M., Rajamäki, M.-L., & Valkonen, J. P. T. (2001). Towards a protein interaction map of potyviruses: protein interaction matrixes of two potyviruses based on the yeast two-hybrid system. Journal of General Virology, 82(4), 935-939. doi:10.1099/0022-1317-82-4-935Lin, L., Shi, Y., Luo, Z., Lu, Y., Zheng, H., Yan, F., … Wu, Y. (2009). Protein–protein interactions in two potyviruses using the yeast two-hybrid system. Virus Research, 142(1-2), 36-40. doi:10.1016/j.virusres.2009.01.006Shen, W., Wang, M., Yan, P., Gao, L., & Zhou, P. (2010). Protein interaction matrix of Papaya ringspot virus type P based on a yeast two-hybrid system. Acta Virologica, 54(1), 49-54. doi:10.4149/av_2010_01_49Redner, S. (2008). Teasing out the missing links. Nature, 453(7191), 47-48. doi:10.1038/453047aIrizarry, R. A. (2003). Exploration, normalization, and summaries of high density oligonucleotide array probe level data. Biostatistics, 4(2), 249-264. doi:10.1093/biostatistics/4.2.249Smyth, G. K. (2004). Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments. Statistical Applications in Genetics and Molecular Biology, 3(1), 1-25. doi:10.2202/1544-6115.1027Allemeersch, J., Durinck, S., Vanderhaeghen, R., Alard, P., Maes, R., Seeuws, K., … Kuiper, M. T. R. (2005). Benchmarking the CATMA Microarray. A Novel Tool forArabidopsis Transcriptome Analysis. Plant Physiology, 137(2), 588-601. doi:10.1104/pp.104.051300Cleveland, W. S. (1979). Robust Locally Weighted Regression and Smoothing Scatterplots. Journal of the American Statistical Association, 74(368), 829-836. doi:10.1080/01621459.1979.10481038Tarraga, J., Medina, I., Carbonell, J., Huerta-Cepas, J., Minguez, P., Alloza, E., … Dopazo, J. (2008). GEPAS, a web-based tool for microarray data analysis and interpretation. Nucleic Acids Research, 36(Web Server), W308-W314. doi:10.1093/nar/gkn303Al-Shahrour, F., Minguez, P., Vaquerizas, J. M., Conde, L., & Dopazo, J. (2005). BABELOMICS: a suite of web tools for functional annotation and analysis of groups of genes in high-throughput experiments. Nucleic Acids Research, 33(Web Server), W460-W464. doi:10.1093/nar/gki456Al-Shahrour, F., Minguez, P., Tárraga, J., Medina, I., Alloza, E., Montaner, D., & Dopazo, J. (2007). FatiGO +: a functional profiling tool for genomic data. Integration of functional annotation, regulatory motifs and interaction data with microarray experiments. Nucleic Acids Research, 35(suppl_2), W91-W96. doi:10.1093/nar/gkm260Mueller, L. A., Zhang, P., & Rhee, S. Y. (2003). AraCyc: A Biochemical Pathway Database for Arabidopsis. Plant Physiology, 132(2), 453-460. doi:10.1104/pp.102.017236Navratil, V., de Chassey, B., Combe, C., & Lotteau, V. (2011). When the human viral infectome and diseasome networks collide: towards a systems biology platform for the aetiology of human diseases. BMC Systems Biology, 5(1), 13. doi:10.1186/1752-0509-5-13Shannon, C. E. (1948). A Mathematical Theory of Communication. Bell System Technical Journal, 27(3), 379-423. doi:10.1002/j.1538-7305.1948.tb01338.
Contrasted Patterns of Molecular Evolution in Dominant and Recessive Self-Incompatibility Haplotypes in Arabidopsis
Self-incompatibility has been considered by geneticists a model system for reproductive biology and balancing selection, but our understanding of the genetic basis and evolution of this molecular lock-and-key system has remained limited by the extreme level of sequence divergence among haplotypes, resulting in a lack of appropriate genomic sequences. In this study, we report and analyze the full sequence of eleven distinct haplotypes of the self-incompatibility locus (S-locus) in two closely related Arabidopsis species, obtained from individual BAC libraries. We use this extensive dataset to highlight sharply contrasted patterns of molecular evolution of each of the two genes controlling self-incompatibility themselves, as well as of the genomic region surrounding them. We find strong collinearity of the flanking regions among haplotypes on each side of the S-locus together with high levels of sequence similarity. In contrast, the S-locus region itself shows spectacularly deep gene genealogies, high variability in size and gene organization, as well as complete absence of sequence similarity in intergenic sequences and striking accumulation of transposable elements. Of particular interest, we demonstrate that dominant and recessive S-haplotypes experience sharply contrasted patterns of molecular evolution. Indeed, dominant haplotypes exhibit larger size and a much higher density of transposable elements, being matched only by that in the centromere. Overall, these properties highlight that the S-locus presents many striking similarities with other regions involved in the determination of mating-types, such as sex chromosomes in animals or in plants, or the mating-type locus in fungi and green algae
Host-symbiont co-speciation and reductive genome evolution in gut symbiotic bacteria of acanthosomatid stinkbugs
- …