Gotowe bibliografie tematyczne / Gene expression profiling

Gotowa bibliografia na temat „Gene expression profiling”

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Data publikacji: 4 czerwca 2021
Data aktualizacji: 1 sierpnia 2024

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Artykuły w czasopismach na temat "Gene expression profiling"

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Frederickson, Robert. "Profiling gene expression". Nature Biotechnology 17, nr 8 (sierpień 1999): 739. http://dx.doi.org/10.1038/11655.

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Kuusisto, Finn. "Gene expression profiling". XRDS: Crossroads, The ACM Magazine for Students 21, nr 4 (27.07.2015): 71. http://dx.doi.org/10.1145/2788538.

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Raetz, Elizabeth A., Philip J. Moos, Aniko Szabo i William L. Carroll. "GENE EXPRESSION PROFILING". Hematology/Oncology Clinics of North America 15, nr 5 (październik 2001): 911–30. http://dx.doi.org/10.1016/s0889-8588(05)70257-4.

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Sotiriou, C., i P. Dinh. "Gene expression profiling". European Journal of Cancer Supplements 6, nr 7 (kwiecień 2008): 105. http://dx.doi.org/10.1016/s1359-6349(08)70508-1.

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Vallente, Rhea. "Boosting Gene Expression Profiling". Genetic Engineering & Biotechnology News 32, nr 20 (15.11.2012): 1–24. http://dx.doi.org/10.1089/gen.32.20.09.

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Dyer,, Randy. "High-Throughput Gene-Expression Profiling". Genetic Engineering & Biotechnology News 31, nr 13 (lipiec 2011): 38–39. http://dx.doi.org/10.1089/gen.31.13.16.

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Gitig, Diana. "Gene-Expression Profiling Finds Niche". Genetic Engineering & Biotechnology News 31, nr 20 (15.11.2011): 24–26. http://dx.doi.org/10.1089/gen.31.20.11.

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Tiwari, Manjul. "Lymphomas: Its gene expression profiling". Journal of Cancer Research and Therapeutics 7, nr 4 (2011): 393. http://dx.doi.org/10.4103/0973-1482.91998.

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Delgado, N., C. Y. Hung, E. Tarcha, M. J. Gardner i G. T. Cole. "Profiling gene expression inCoccidioides posadasii". Medical Mycology 42, nr 1 (styczeń 2004): 59–71. http://dx.doi.org/10.1080/1369378031000156890.

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Snell, Terry W., Sara E. Brogdon i Michael B. Morgan. "Gene Expression Profiling in Ecotoxicology". Ecotoxicology 12, nr 6 (grudzień 2003): 475–83. http://dx.doi.org/10.1023/b:ectx.0000003033.09923.a8.

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Rozprawy doktorskie na temat "Gene expression profiling"

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Muszynska, Dorota. "Gene expression profiling in Keratoconus". Thesis, Queen's University Belfast, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.602693.

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Keratoconus (MIM#148300), a common bilateral, progressive corneal thinning disorder, is the leading indication for corneal transplantation in the developed world. Keratoconus usually arises in the teenage years and presents a significant health burden in work-age adults. Despite the visual and social impact of keratoconus, our lack of understanding of the molecular pathology of keratoconus is a major obstacle to the development of new therapeutic approaches. This study represents the first reported application of massively parallel sequencing of mRNA (RNA-Seq) to perform whole genome transcriptome analysis of keratoconic keratocytes. Genes-enrichment analysis identified several pathway maps that are disrupted in keratoconic keratocytes and associated with the pathogenesis of keratoconus. Microarray gene expression was used to validate differentially expressed genes identified by RNA-Seq in a global manner, whereas quantitative reverse transcriptase polymerase chain reaction was performed on selected candidate genes. Wnt signalling, TGF-beta signalling. ECM-matrix interactions, oxidative stress and inflammatory- related genes were specifically identified in keratoconic keratocytes and implicated in the pathogenesis of keratoconus. Analysis of individual target genes identified altered expression of both known and novel keratoconus-related genes, in particular, SFRP1, BMP4, CBS, POSTN, C0L11Al, COL4Al, SOD1, IL6, and SP3. Functional analyses and expression profiling of keratoconic keratocytes harbouring a novel heterozygous missense mutation (c.l920G>T; p.Gln640His) in the zinc finger E-box binding gene 1 (ZEB1) was also performed. The mutant ZEB1 protein was stable and localised to the nucleus resulting in an enhanced transcriptional repressor of known ZEB1 targets, involved in epithelialmesenchymal transition and collagen synthesis. This ZEB1 mutation results in a gain-In-function with enhanced transcriptional repression of a number of gene targets associated with keratoconus, corneal thickness and Fuchs endothelial corneal dystrophy. This study has identified a number of molecular targets for keratoconus and provides a significant insight into the gene pathways involved in keratoconus pathogenesis. Further functional studies can build on this evidence to interrogate disease pathogenesis, identify novel genes and develop molecular therapies for keratoconus.
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Leonard, Pauline Catherine. "Gene expression profiling of osteosarcoma". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445814/.

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Purpose: The aim of the work described in this thesis was to determine whether needle core and open biopsies from osteosarcoma (OS) provide sufficient quality of mRNA for cDNA array analyses which might then provide insights into the expression profile of OS. Experimental Design: Sixteen samples collected from OS and two established cell lines were used for array analyses. A primary cell culture was also established from one of the OS biopsies. Total RNA was extracted and probes generated for cDNA arrays. A reference probe was included for computational analyses. Results: cDNA probes were made for twenty five samples. Two of these samples were needle core bone biopsies. Twenty two cDNA probes were used for the generation of microarray data. Previous established statistical analysis confirmed the reliability of array data obtained in sixteen of the twenty two samples. Known genes involved in bone metabolism, osteoblast differentiation and cancer cell growth, were identified as up- or down-regulated in OS. Conclusions: Without amplification of RNA, OS tissue including small core bone biopsies, are amenable to cDNA array analysis. Known and novel putative markers for OS, that could have prognostic value, were identified.
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Hägg, Sara. "Gene Expression Profiling of Human Atherosclerosis". Doctoral thesis, Linköpings universitet, Biologiska Beräkningar, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-52085.

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Atherosclerosis is a progressive inflammatory disease that causes lipid accumulation in the arterial wall, leading to the formation of plaques. The clinical manifestations of plaque rupture—stroke and myocardial infarction—are increasing worldwide and pose an enormous economic burden for society. Atherosclerosis development reflects a complex interaction between environmental exposures and genetic predisposition. To understand this complexity, we hypothesized that a top-down approach—one in which all molecular activities that drive atherosclerosis are examined simultaneously—is necessary to highlight those that are clinically relevant. To this end, we performed whole-genome expression profiling in multiple tissues isolated from patients with coronary artery disease (CAD). In the Stockholm Atherosclerosis Gene Expression (STAGE) study, biopsies of five tissues (arterial wall with and without atherosclerotic lesions, liver, skeletal muscle and visceral fat) were isolated from 124 CAD patients undergoing coronary artery bypass grafting surgery (CABG) at the Karolinska University Hospital, Solna and carotid lesions from 39 patients undergoing carotid artery surgery at Stockholm Söder Hospital. Detailed clinical characteristics of these patients were assembled together with a total of 303 global gene expression profiles obtained with the Affymetrix GeneChip platform. In paper 1, a two-way clustering analysis of the data identified 60 tissue clusters of functionally related genes. One cluster, partly present in both visceral fat and atherosclerotic lesions, related to atherosclerosis severity as judged by coronary angiograms. Many of the genes in that cluster were also present in a carotid lesion cluster relating to intima-media thickness (IMT) in the carotid patients. The union of all three clusters relating to extent of atherosclerosis—referred to as the “A-module”—was overrepresented with genes belonging to the transendothelial migration of leukocyte (TEML) pathway. The transcription co-factor, Lim domain binding 2 (LDB2), was identified as putative regulator of the A-module and TEML pathway in validation studies including Ldb2-/- mice. In paper 2, we investigated the increased incidence of postoperative complications in CABG patients with diabetes. Using the STAGE compendium, we identified an anti-inflammatory marker, dual-specificity phosphatase 1 (DUSP1), as a novel preoperative blood marker of risk for a prolonged hospital stay after CABG. In paper 3, plaque age was determined with C14-dating in the carotid patients. Interestingly, the strongest correlation with plaque age was not the age of the patients or IMT. Rather, the strongest correlations were with plasma insulin levels and inflammatory gene expression. Taken together, the findings in this thesis show that a top-down approach using multi-tissue gene expression profiling in CAD and C14-dating of plaques can contribute to a better understanding of the molecular processes underlying atherosclerosis development and to the identification of clinically useful biomarkers.
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Bain, Peter A., i n/a. "Gene Expression Profiling of Cylindrospermopsin Toxicity". Griffith University. School of Biomolecular and Physical Sciences, 2007. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20080404.145834.

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Cylindrospermopsin (CYN) is a toxic alkaloid produced by several freshwater cyanobacterial species, the most prevalent in Australian waters being Cylindrospermopsis raciborskii. The occurrence of CYN-producing cyanobacteria in drinking water sources worldwide poses a potential human health risk, with one well-documented case of human poisoning attributed to the toxin. While extensive characterisation of CYN-induced toxicity has been conducted in rodents both in vivo and in primary cell cultures, little is known about mechanisms of toxicity in human cell types. This thesis describes studies undertaken to further define the molecular mechanisms of CYN toxicity in human cells. Concentration-response relationships were determined in various cultured human cell types using standard toxicity assays. As expected, CYN caused dose-dependent decreases in the growth of three cell lines, HepG2, Caco-2 and HeLa, and one primary cell type, human dermal fibroblasts, according to tetrazolium reduction assays. CYN treatment did not disrupt cellular membranes according to the lactate dehydrogenase release assay in HepG2 or Caco-2 cells after 24, 48 or 72 h exposure, but did cause membrane disruption in fibroblasts after 72 h exposure to relatively high concentrations of the toxin. Apoptosis occurred more readily in HeLa cells than HepG2 cells or fibroblasts, with 72 h exposure to 1 &mug/mL required before statistically significant rates of apoptosis occurred in the latter cell types. CYN did not appear to directly affect the structure of actin filaments or microtubules under the conditions used in the present study. The major portion of the work presented in this thesis comprises a large-scale interrogation of changes in gene expression induced by the toxin in cultured cells. To assess the effects of CYN on global gene expression, relative messenger RNA (mRNA) levels in human dermal fibroblasts and HepG2 cells after 6 h and 24 h exposure to 1 &mug/mL CYN were determined using oligonucleotide microarrays representing approximately 19 000 genes. Overall, the number of transcripts significantly altered in abundance was greater in fibroblasts than in HepG2 cells. In both cell types, mRNA levels for genes related to amino acid biosynthesis, carbohydrate metabolism, and protein folding and transport were reduced after CYN treatment, while transcripts representing genes for apoptosis, RNA biosynthesis and RNA processing increased in abundance. More detailed data analyses revealed the modulation of a number of stress response pathways—genes regulated by NF-&kappaB were induced, DNA damage response pathways were up-regulated, and a large number of genes involved in endoplasmic reticulum stress were strongly down-regulated. Genes for the synthesis and processing of mRNA, tRNA and rRNA were strongly up-regulated, indicating that CYN treatment may increase the turnover of all forms of cellular RNA. A small group of genes were differentially expressed in HepG2 cells and fibroblasts, revealing cell-specific responses to the toxin. Selected changes in transcript level were validated using real-time quantitative reverse transcriptase PCR (qRT-PCR). The modulation of stress response pathways by CYN, indicated by microarray analysis, was further investigated using other methods. The role of tumour suppressor protein p53 in CYN-mediated gene expression was confirmed by measuring the expression of known p53-regulated genes following CYN treatment of HepG2 cells and human dermal fibroblasts using qRT-PCR. Western blotting of protein extracts from CYNtreated cells showed that p53 protein accumulation occurred in HepG2 cells, providing additional evidence of the activation of the p53 pathway by CYN in this cell line. The immediate-early genes JUN and FOS were found to be induced by CYN in a concentration-dependent manner, and MYC was induced to a lesser extent. The mitogen-activated protein kinase c-Jun NH2-terminal kinase, implicated in the ribotoxic stress response initiated by damage to ribosomal RNA, appeared to become phosphorylated in HeLa cells after CYN exposure, suggesting that ribotoxic stress may occur in response to CYN in at least some cell types. The expression of a reporter gene under the control of a response element specific for NF-&kappaB was induced at the mRNA level but inhibited at the protein level. This shows that while transcription factors such as p53 and NF-&kappaB are apparently activated in response to the toxin, transactivation of target genes may not necessarily manifest a corresponding increase at the protein level. The current work contributes significantly to the current understanding of cylindrospermopsin toxicity in human-derived cell types, and provides further insight into putative modes of action.
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Beijnum, Judith Rosina van. "Gene expression profiling of tumor angiogenesis". Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7710.

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Al-Halabi, Hani. "Gene expression profiling in adult Medulloblastoma". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107616.

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Medulloblastoma (MB) represents approximately 1% of adult brain tumours, and as such is a poorly studied disease. It exhibits different clinical manifestations and outcome in adults, yet it is still treated as per pediatric protocols. Recently, gene expression profiling studies suggested the existence of at least 4 molecular subtypes in pediatric MB, characterized by distinct genetic profiles, activation of oncogenic pathways and varied clinical outcomes. This has refined our ability to classify MB, select tumors for targeted therapy and is leading the way to individualized medicine. It is unknown whether adult MB has its unique molecular signature and whether biologic differences underlie the clinical discrepancies observed in the adult population. We hypothesized that MB displays age-related biological differences and to further characterize these differences; we studied the gene expression profiles of a cohort of adult MB and compared them to a pediatric MB dataset. We found a preponderance of SHH pathway activation amongst adult MB tumours (26/31, 84%). This is in support with evolving data that have identified SHH signature in 75% of adult MB. In view of reports on the good clinical response observed with the use of selective SHH inhibitors in SHH driven MB, our results suggest that the adjuvant use of these agents may improve outcomes in adult MB and should be investigated within a prospective trial. Sonic hedgehog active adult MB represent a homogenous tumor population, which exhibits differences in molecular profiles compared to pediatric SHH driven MB. The later potentially explains the variable outcome between adults and infants with SHH MB, and outlines potential targets of MB tumorigenesis in adults. This thesis offers new insights into age based molecular differences in MB and highlights adult patients as potential targets for selective therapy targeting the SHH pathway.
Le médulloblastome (MB) représente environ 1% des tumeurs du cerveau adulte, et en tant que telle est une maladie peu étudiée. Il présente différentes manifestations cliniques et differents résultats chez les adultes, mais il est encore traité selon les protocoles pédiatriques. Récemment, des études d'expression de profil génétique suggére l'existence d'au moins 4 sous-types moléculaires pour le MB pédiatriques, caractérisées par des profils génétiques distincts, par l'activation des voies de signallisation oncogéniques et par des résultats cliniques variées. Cela a amélioré notre capacité de classifier le MB, a mieux sélectionné les tumeurs pour le traitement ciblé et ouvre la voie à une médecine individualisée. On ignore si le MB adulte possede une signature moléculaire unique et si ce sont des différences biologiques qui expliquent les différences cliniques observées dans la population adulte. Nous proposons que le MB possede des différences biologiques qui varie en fonction de l'âge et afin de mieux caractériser ces différences, nous avons étudié les profils d'expression génetique d'une cohorte de MB adultes et les ont comparés à une base de données de MB pédiatrique. Nous avons trouvé une prépondérance d'activation de la voie SHH parmi les tumeurs de MB adulte (26/31, 84%). Ceci supporte les données qui ont identifié la signature SHH dans 75% des MB adultes. Compte tenu des rapports sur la bonne réponse clinique observée avec l'utilisation d'inhibiteurs sélectifs de Shh dans le MB à SHH, nos résultats suggèrent que l'utilisation adjuvante de ces agents peut améliorer les résultats pour le MB adulte et devrait être étudiée dans une étude prospective. Le MB adulte avec Sonic hedgehog actif représente une population homogène de tumeur, et présente des différences dans les profils moléculaires par rapport au MB pédiatriques à SHH. Cela pourrait expliquer les résultat variable entre adultes et enfants avec le MB à SHH, et décrit des cibles potentielles de la tumorogenèse du MB chez les adultes. Cette thèse propose de nouveaux aperçus sur l'effet de l'âge sur les différences moléculaires pour le MB et met en évidence que les patients adultes representent des cibles potentielles pour la thérapie de ciblage sélectif de la voie SHH.
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Goh, Huey Tse. "Profiling cardiac gene expression during endotoxaemia". Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.523087.

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Brooks, W. M. "Profiling gene expression in Alzheimer's disease". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596943.

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Alzheimer’s disease is a debilitating neurodegenerative disease expected to increase in prevalence during the next few decades. Familial Alzheimer’s disease cases have revealed some molecules that appear to be involved in the disease pathogenesis. However, factors fully explaining the vast majority of case of Alzheimer’s disease which are sporadic, wait to be determined. The present study conducted a broad survey of gene expression in Alzheimer’s disease post mortem tissue with the aim of identifying gene expression products involved in this disease. Initially, a study was carried out to determine the effects of post mortem interval on gene expression assessment by cDNA array hybridisation. This study used mouse tissue in which the post mortem delay prior to freezing could be controlled. Observations from this study led to the conclusion that it is acceptable to assess gene expression in samples with varying PMIs. Samples derived from Alzheimer diseased and control human post mortem tissues were then compared to reveal differences in gene expression at the RNA level. The brain area under investigation was the hippocampus which is important for memory and is known to be affected in Alzheimer’s disease. Initially, five samples (2 Alzheimer’s disease, 3 controls) were screened against Affymetrix GeneChip HG-U133A arrays . The findings from this study were used, along with findings reported by other researchers, to identify candidates whose expression appeared to be altered in Alzheimer’s disease. Semi-quantitative Real-Time PCR was used to verify differential expression of the genes of interest in a greater number of samples (6 Alzheimer’s disease, 5 controls). This resulted in the identification of 13 statistically significant differentially expressed genes in Alzheimer’s disease from the 67 investigated. These included transcripts involved in ubiquitination, neurotransmission and energy metabolism amongst others. The biological significance of these findings is discussed.
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Cleator, Susan Jane. "Gene expression profiling of breast cancers". Thesis, Institute of Cancer Research (University Of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423120.

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Bain, Peter A. "Gene Expression Profiling of Cylindrospermopsin Toxicity". Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367068.

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Cylindrospermopsin (CYN) is a toxic alkaloid produced by several freshwater cyanobacterial species, the most prevalent in Australian waters being Cylindrospermopsis raciborskii. The occurrence of CYN-producing cyanobacteria in drinking water sources worldwide poses a potential human health risk, with one well-documented case of human poisoning attributed to the toxin. While extensive characterisation of CYN-induced toxicity has been conducted in rodents both in vivo and in primary cell cultures, little is known about mechanisms of toxicity in human cell types. This thesis describes studies undertaken to further define the molecular mechanisms of CYN toxicity in human cells. Concentration-response relationships were determined in various cultured human cell types using standard toxicity assays. As expected, CYN caused dose-dependent decreases in the growth of three cell lines, HepG2, Caco-2 and HeLa, and one primary cell type, human dermal fibroblasts, according to tetrazolium reduction assays. CYN treatment did not disrupt cellular membranes according to the lactate dehydrogenase release assay in HepG2 or Caco-2 cells after 24, 48 or 72 h exposure, but did cause membrane disruption in fibroblasts after 72 h exposure to relatively high concentrations of the toxin. Apoptosis occurred more readily in HeLa cells than HepG2 cells or fibroblasts, with 72 h exposure to 1 µg/mL required before statistically significant rates of apoptosis occurred in the latter cell types. CYN did not appear to directly affect the structure of actin filaments or microtubules under the conditions used in the present study. The major portion of the work presented in this thesis comprises a large-scale interrogation of changes in gene expression induced by the toxin in cultured cells. To assess the effects of CYN on global gene expression, relative messenger RNA (mRNA) levels in human dermal fibroblasts and HepG2 cells after 6 h and 24 h exposure to 1 µg/mL CYN were determined using oligonucleotide microarrays representing approximately 19 000 genes. Overall, the number of transcripts significantly altered in abundance was greater in fibroblasts than in HepG2 cells. In both cell types, mRNA levels for genes related to amino acid biosynthesis, carbohydrate metabolism, and protein folding and transport were reduced after CYN treatment, while transcripts representing genes for apoptosis, RNA biosynthesis and RNA processing increased in abundance. More detailed data analyses revealed the modulation of a number of stress response pathways—genes regulated by NF-?B were induced, DNA damage response pathways were up-regulated, and a large number of genes involved in endoplasmic reticulum stress were strongly down-regulated. Genes for the synthesis and processing of mRNA, tRNA and rRNA were strongly up-regulated, indicating that CYN treatment may increase the turnover of all forms of cellular RNA. A small group of genes were differentially expressed in HepG2 cells and fibroblasts, revealing cell-specific responses to the toxin. Selected changes in transcript level were validated using real-time quantitative reverse transcriptase PCR (qRT-PCR). The modulation of stress response pathways by CYN, indicated by microarray analysis, was further investigated using other methods. The role of tumour suppressor protein p53 in CYN-mediated gene expression was confirmed by measuring the expression of known p53-regulated genes following CYN treatment of HepG2 cells and human dermal fibroblasts using qRT-PCR. Western blotting of protein extracts from CYNtreated cells showed that p53 protein accumulation occurred in HepG2 cells, providing additional evidence of the activation of the p53 pathway by CYN in this cell line. The immediate-early genes JUN and FOS were found to be induced by CYN in a concentration-dependent manner, and MYC was induced to a lesser extent. The mitogen-activated protein kinase c-Jun NH2-terminal kinase, implicated in the ribotoxic stress response initiated by damage to ribosomal RNA, appeared to become phosphorylated in HeLa cells after CYN exposure, suggesting that ribotoxic stress may occur in response to CYN in at least some cell types. The expression of a reporter gene under the control of a response element specific for NF-?B was induced at the mRNA level but inhibited at the protein level. This shows that while transcription factors such as p53 and NF-?B are apparently activated in response to the toxin, transactivation of target genes may not necessarily manifest a corresponding increase at the protein level. The current work contributes significantly to the current understanding of cylindrospermopsin toxicity in human-derived cell types, and provides further insight into putative modes of action.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Faculty of Science, Environment, Engineering and Technology
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Książki na temat "Gene expression profiling"

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Shimkets, Richard A. Gene Expression Profiling. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592597513.

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O'Driscoll, Lorraine, red. Gene Expression Profiling. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-289-2.

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A, Shimkets Richard, red. Gene expression profiling: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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A, Lidbury Brett, i Mahalingam Suresh, red. Gene profiling in drug design. Boca Raton: Taylor & Francis, 2008.

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Wang, Zhiguo. MicroRNA expression detection methods. Heidelberg: Springer, 2010.

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Marc, Ladanyi, i Gerald William L, red. Expression profiling of human tumors: Diagnostic and research applications. Totowa, N.J: Humana Press, 2003.

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Marc, Ladanyi, i Gerald William L, red. Expression profiling of human tumors: Diagnostic and research applications. Totowa, N.J: Humana Press, 2003.

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Luigi, Marchionni, United States. Agency for Healthcare Research and Quality. i Johns Hopkins University. Evidence-based Practice Center., red. Impact of gene expression profiling tests on breast cancer outcomes. Rockville, MD: Agency for Healthcare Research and Quality, 2008.

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Phillip, Stafford, red. Methods in microarray normalization. Boca Raton: CRC Press, 2008.

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1940-, Hatfield G. Wesley, red. DNA microarrays and gene expression. New York: Cambridge University Press, 2002.

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Części książek na temat "Gene expression profiling"

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Druka, Arnis, Robbie Waugh i Pete Hedley. "Gene Expression Profiling". W Springer Protocols Handbooks, 195–211. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-375-6_14.

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Dunphy, Cherie H. "Gene Expression Profiling". W Molecular Pathology Library, 177–89. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5698-9_13.

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Hasson, Brian F., Brandon J. Fisher, Larry C. Daugherty, Brandon J. Fisher, Larry C. Daugherty, Filip T. Troicki, Jaganmohan Poli i in. "Gene Expression Profiling". W Encyclopedia of Radiation Oncology, 297. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_612.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier i in. "Gene Expression Profiling". W Encyclopedia of Exercise Medicine in Health and Disease, 360. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2428.

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Pathania, Amit, i Vijaykumar Yogesh Muley. "Gene Expression Profiling". W Encyclopedia of Animal Cognition and Behavior, 1–6. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_9-1.

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Pathania, Amit, i Vijaykumar Yogesh Muley. "Gene Expression Profiling". W Encyclopedia of Animal Cognition and Behavior, 2882–87. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_9.

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Gilbert, Jack A., i Margaret Hughes. "Gene Expression Profiling: Metatranscriptomics". W Methods in Molecular Biology, 195–205. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-089-8_14.

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Zhou, Yu, Chao Xu, Jigang Zhang i Hong-Wen Deng. "Gene Expression and Profiling". W Translational Bioinformatics, 59–82. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7543-4_3.

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LéDée, Nathalie. "Endometrial Immune Profiling: An Emerging Paradigm for Reproductive Disorders". W Endometrial Gene Expression, 75–89. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28584-5_5.

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Asmann, Yan W., E. Aubrey Thompson i Jean-Pierre A. Kocher. "Gene Expression Profiling Using 3′ Tag Digital Approach". W Expression Profiling in Neuroscience, 77–87. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-448-3_5.

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Streszczenia konferencji na temat "Gene expression profiling"

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Jin, Rui, Xue-mei Ma, Peng-xiang Zhao, Juan Feng, Li-ning Guo, Ru-gang Zhong, Yi Zeng, Jian-min Ma, Ji-tong Shi i Xin Ge. "Gene Expression Profiling of Idiopathic Orbital Inflammatory Pseudotumors". W 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5516934.

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Hersh, CP, T. Betsuyaku, N. Patel, N. Marchetti, BJ Klanderman, VJ Carey, GJ Criner i AM Choi. "Alveolar-Specific Gene Expression Profiling in Emphysematous Lungs." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1892.

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Zhou, Tong, Wei Zhang, Shwu-Fan Ma, Michael S. Wade, Imre Noth i Joe G. N. Garcia. "Profiling Of Gene Expression In Idiopathic Pulmonary Fibrosis". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4924.

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VAN DYK, TINA K., GREGORY E. GONYE, MARY JANE G. REEVE, ELLEN J. DEROSE, MAUREEN DOLAN, MICHAEL K. HANAFEY, YAN WEI, J. ANTONI RAFALSKI i ROBERT A. LAROSSA. "GENOME-WIDE EXPRESSION PROFILING WITH luxCDABE GENE FUSIONS". W Proceedings of the 11th International Symposium. WORLD SCIENTIFIC, 2001. http://dx.doi.org/10.1142/9789812811158_0112.

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Haifeng Li, Keshu Zhang i Tao Jiang. "Robust and accurate cancer classification with gene expression profiling". W 2005 IEEE Computational Systems Bioinformatics Conference (CSB'05). IEEE, 2005. http://dx.doi.org/10.1109/csb.2005.49.

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Thompson, Anna R., Samantha A. Natanek, Saffron A. Willis-Owen, William O. Cookson, Michael I. Polkey i Miriam F. Moffatt. "Gene Expression Profiling Of Quadriceps Femoris Muscle In COPD". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4259.

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Spears, Melanie, Vida Talebian, Linda Liao, Megan Hopkins, Drashti Jain, Mary Anne Quintayo, Jane Bayani, Alison Cheung, Martin Yaffe i John M. Bartlett. "Abstract 2698: Spatial gene expression profiling in breast cancer". W Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2698.

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van Lunteren, Erik, i Michelle Moyer. "Lung Gene Expression Profiling In Type 2 Diabetic Rats". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2138.

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Baines, Katherine J., Jodie L. Simpson, Rodney J. Scott, Lisa G. Wood i Peter Gibson. "Molecular Phenotypes Of Asthma Defined By Gene Expression Profiling". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5097.

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Willems, B., P. Ströhle, L. Robbel, M. Broxtermann, S. Bienert i M. Gajewski. "Gene-expression profiling during embryogenesis of Zebrafish under microgravity conditions". W 57th International Astronautical Congress. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2006. http://dx.doi.org/10.2514/6.iac-06-a1.4.06.

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Raporty organizacyjne na temat "Gene expression profiling"

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Marchionni, Luigi, Renee F. Wilson, Spyridon S. Marinopoulos, Antonio C. Wolff, Giovanni Parmigiani, Eric B. Bass i Steven N. Goodman. Impact of Gene Expression Profiling Tests on Breast Cancer Outcomes. Agency for Healthcare Research and Quality, styczeń 2008. http://dx.doi.org/10.23970/ahrqepcerta160.

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Xiaoliang Sunney Xie. Real-Time Gene Expression Profiling of Live Shewanella Oneidensis Cells. Office of Scientific and Technical Information (OSTI), marzec 2009. http://dx.doi.org/10.2172/950422.

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Geiss, K. T., i J. M. Frazier. Toxicity of Experimental Jet Fuel System Ice-Inhibiting Agents: 2. Gene Expression Response Profiling. Fort Belvoir, VA: Defense Technical Information Center, maj 1999. http://dx.doi.org/10.21236/ada453166.

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Xie, Xiao-Li. Identification of Key Genes and Pathways in First Acute Myocardial Infarction Based on Gene Expression Profiling by Bioinformatics Analysis. Science Repository, czerwiec 2019. http://dx.doi.org/10.31487/j.jicoa.2019.02.02.

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Hiyama, Eiso. Gene expression profiling in hepatoblastoma cases of the Japanese Study Group for Pediatric Liver Tumors-2 (JPLT-2) trial. Science Repository OU, luty 2019. http://dx.doi.org/10.31487/j.ejmc.2018.01.003.

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Grumet, Rebecca, Rafael Perl-Treves i Jack Staub. Ethylene Mediated Regulation of Cucumis Reproduction - from Sex Expression to Fruit Set. United States Department of Agriculture, luty 2010. http://dx.doi.org/10.32747/2010.7696533.bard.

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Reproductive development is a critical determinant of agricultural yield. For species with unisexual flowers, floral secualdifferentation adds additional complexity, that can influenec productivity. The hormone ethylene has long, been known to play a primary role in sex determination in the Cucumis species cucumber (C. sativus) and melon (C. melo). Our objectives were to: (1) Determine critical sites of ethylene production and perception for sex determination; (2) Identify additional ethylene related genes associated with sex expression; and (3) Examine the role of environment ami prior fruit set on sex expression, pistillate flower maturation, and fruit set. We made progress in each of these areas. (1) Transgenic melon produced with the Arabidopsis dominant negative ethylene perception mutant gene, etrl-1, under the control of floral primordia targeted promoters [AP3 (petal and stamen) and CRC (carpel and nectary)], showed that ethylene perception by the stamen primordia, rather than carpel primordia, is critical for carpel development at the time of sex determination. Transgenic melons also were produced with the ethylene production enzyme gene. ACS, encoding l-aminocyclopropane-lcarboylate synthase, fused to the AP3 or CRC promoters. Consistent with the etr1-1 results, CRC::ACS did not increase femaleness; however, AP3::ACS reduced or eliminated male flower production. The effects of AP3:ACS were stronger than those of 35S::ACS plants, demonstratin g the importance of targeted expression, while avoiding disadvantages of constitutive ethylene production. (2) Linkage analysis coupled with SNP discovery was per formed on ethylene and floral development genes in cucumber populations segregating for the three major sex genes. A break-through towards cloning the cucumber M gene occurred when the melon andromonoecious gene (a), an ACS gene, was cloned in 2008. Both cucumber M and melon a suppress stamen development in pistillate flowers. We hypothesized that cucumber M could be orthologous to melon a, and found that mutations in CsACS2 co-segregated perfectly with the M gene. We also sought to identify miRNA molecules associated with sex determination. miRNA159, whose target in Arabidopsis is GAMYB[a transcription factor gene mediating response to10 gibberellin (GA)], was more highly expressed in young female buds than male. Since GA promotes maleness in cucumber, a micro RNA that counteracts GAMYB could promote femaleness. miRNA157, which in other plants targets transcription factors involved in flower development , was expressed in young male buds and mature flower anthers. (3) Gene expression profiling showed that ethylene-, senescence-, stress- and ubiquitin-related genes were up-regulated in senescing and inhibited fruits, while those undergoing successful fruit set up-regulated photosynthesis, respiration and metabolic genes. Melon plants can change sex expression in response to environmental conditions, leading to changes in yield potential. Unique melon lines with varying sex expression were developed and evaluated in the field in Hancock, Wisconsin . Environmental changes during the growing season influenced sex expression in highly inbred melon lines. Collectively these results are of significance for understanding regulation of sex expression. The fact that both cucumber sex loci identified so far (F and M) encode isoforms of the same ethylene synthesis enzyme, underscores the importance of ethylene as the main sex determining hormone in cucumber. The targeting studies give insight into developmental switch points and suggest a means to develop lines with earlier carpel-bearing flower production and fruit set. These results are of significance for understanding regulation of sex expression to facilitate shorter growing seasons and earlier time to market. Field results provide information for development of management strategies for commercial production of melon cultivars with different sex expression characteristics during fruit production.
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Xu, Jin-Rong, i Amir Sharon. Comparative studies of fungal pathogeneses in two hemibiotrophs: Magnaporthe grisea and Colletotrichum gloeosporioides. United States Department of Agriculture, maj 2008. http://dx.doi.org/10.32747/2008.7695585.bard.

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Plant pathogenic fungi have various life styles and different plant infection strategies. Hemibiotrophs like Magnaporthe grisea and Colletotrichum species develop specialized structures during plant infection. The goal of this study was to identify, characterize, and compare genes required for plant infection in M. grisea and C. gloeosporioides. Specific objectives are to: 1) further characterize genes identified in the preliminary studies of C. gloeosporioides and M. grisea;2) identify and characterize additional fungal genes tagged by GFP; and 3) identify in planta growth and appressorium-specific genes by subtractive hybridization and transcript profiling by the LongSAGE method. In this study, the PI and Co-PI collaborated closely on studies in M. grisea and C. gloeosporioides. In M. grisea, REMI and ATMT were used to transform the wildtype with promoter-less EGFP constructs. A total of 28 mutants defective in different plant infection processes or expressing EGFP during plant infection were identified. Genes disrupted in five selected mutants have been identified, including MG03295 that encodes a putative Rho GTPase. In transformant L1320, the transforming vector was inserted in the MIRI gene that encodes a nuclear protein. The expression of MIRI was highly induced during infection. Deletion and site-directed mutagenesis analyses were used to identify the promoter regions and elements that were essential for induced in planta expression of MIRI. This was the first detailed characterization of the promoter of an in planta gene in M. grisea and the MIRI promoter can be used to monitor infectious growth. In addition, the Agilent whole-genome array of M. grisea was used for microarray analyses with RNA samples from appressoria formed by the wild-type shain and the pmkl and mstl2 mutants. Over 200 genes were downregulated in the mst I 2 and pmkl mutants. Some of them are putative transcription factors that may regulate appressorium formation and infectious hyphal growth. In C. gloeosporioides, various REMI mutants showing different pathogenic behavior were identified and characterized. Mutants N3736 had a single insertion and was hyper-virulent. The gene disrupted in mutant3736 (named CgFMOI) encodes a FAD-dependent monooxygenase. Expression analyses linked the expression of the CgFMOI gene with the necrotrophic phase of fungal infection, and also suggest that expression of CgFMOl is unnecessary for the first stages of infection and for biotrophy establishment. All CgFMOl-silenced mutants had reduced virulence. In REMI mutant N159, the tagged gene encodes a putative copper transporter that is homologue of S. cerevisiae CTR2. In yeast, Ctr2 is a vacuolar transporter for moving copper from the vacuole to the cytoplasm. The gene was therefore termed CgCTR2. In addition to characterization of CgCTR2, we also conducted comparative analyses in M. grisea. The M. grisea CgCTR-2 homolog was isolated, knockout strains were generated and characterized and the M. grisea was used to complement the Nl 59 C. gloeosporioides mutant. Overall, we have accomplished most of proposed experiments and are in the process of organizing and publishing other data generated in this project. For objective 3, we used the microarray analysis approach. Several genes identified in this study are novel fungal virulence factors. They have the potential to be used as targets for developing more specific or effective fungicides. In the long run, comparative studies of fungal genes, such as our CgCTR2 work, may lead to better disease control strategies.
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Ori, Naomi, i Mark Estelle. Specific mediators of auxin activity during tomato leaf and fruit development. United States Department of Agriculture, styczeń 2012. http://dx.doi.org/10.32747/2012.7597921.bard.

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The plant hormone auxin is involved in numerous developmental processes, including leaf and fruit development. The tomato (Solanumlycopersicum) gene ENTIRE (E) encodes an auxin-response inhibitor from the Aux/IAA family. While most loss-offunction mutations in Aux/IAA genes are similar to the wild type due to genetic redundancy, entire (e) mutants show specific effects on leaf and fruit development. e mutants have simple leaves, in contrast to the compound leaves of wild type tomatoes. In addition, e plants produce parthenocarpic fruits, in which fruit set occurs independently of fertilization. The aim of this research program was to utilize the e mutation to identify and characterize genes that mediate the specific effect of auxin in leaf and fruit development. The specific objectives of the project were to: 1. Characterize and map modifiers of the e leaf phenotype. 2. Characterize and map suppressors of the e fruit phenotype. 3. Dissect the developmental specificity of the E gene. 4. Examine the effect of fruit-overexpression of identified genes on fruit set and seed production. To identify mediators of auxin in leaf development, we mainly focused on one mutant, crawling elephant (crel, previously called t282), which showed substantial suppression of the e phenotype and other auxin-relatedphenotypes. We have identified the CREL gene as a homolog of the Arabidopsis VRN5 gene, involved in recruiting polycomb silencing complexes to specific targets. We showed that CREL affects auxin sensitivity in tomato. Suppressors of the e fruit phenotype have been further characterized and selected for more profound effects. Expression profiling by RNAseq was used to analyze the effect of e as well as crel on gene expression in leaves and fruits. This analysis has identified putative E and CREL targets. We have initiated studies to assess the role of some of these targets in flower and fruit development. The research has identified potential mediators of auxin response in leaf, flower and fruit development.
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Aharoni, Asaph, Zhangjun Fei, Efraim Lewinsohn, Arthur Schaffer i Yaakov Tadmor. System Approach to Understanding the Metabolic Diversity in Melon. United States Department of Agriculture, lipiec 2013. http://dx.doi.org/10.32747/2013.7593400.bard.

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Fruit quality is determined by numerous genetic factors that affect taste, aroma, ‎color, texture, nutritional value and shelf life. To unravel the genetic components ‎involved in the metabolic pathways behind these traits, the major goal of the project was to identify novel genes that are involved in, or that regulate, these pathways using correlation analysis between genotype, metabolite and gene expression data. The original and specific research objectives were: (1) Collection of replicated fruit from a population of 96 RI lines derived from parents distinguished by great diversity in fruit development and quality phenotypes, (2) Phenotypic and metabolic profiling of mature fruit from all 96 RI lines and their parents, (3) 454 pyrosequencing of cDNA representing mRNA of mature fruit from each line to facilitate gene expression analysis based on relative EST abundance, (4) Development of a database modeled after an existing database developed for tomato introgression lines (ILs) to facilitate online data analysis by members of this project and by researchers around the world. The main functions of the database will be to store and present metabolite and gene expression data so that correlations can be drawn between variation in target traits or metabolites across the RI population members and variation in gene expression to identify candidate genes which may impact phenotypic and chemical traits of interest, (5) Selection of RI lines for segregation and/or hybridization (crosses) analysis to ascertain whether or not genes associated with traits through gene expression/metabolite correlation analysis are indeed contributors to said traits. The overall research strategy was to utilize an available recombinant inbred population of melon (Cucumis melo L.) derived from phenotypically diverse parents and for which over 800 molecular markers have been mapped for the association of metabolic trait and gene expression QTLs. Transcriptomic data were obtained by high throughput sequencing using the Illumina platform instead of the originally planned 454 platform. The change was due to the fast advancement and proven advantages of the Illumina platform, as explained in the first annual scientific report. Metabolic data were collected using both targeted (sugars, organic acids, carotenoids) and non-targeted metabolomics analysis methodologies. Genes whose expression patterns were associated with variation of particular metabolites or fruit quality traits represent candidates for the molecular mechanisms that underlie them. Candidate genes that may encode enzymes catalyzingbiosynthetic steps in the production of volatile compounds of interest, downstream catabolic processes of aromatic amino acids and regulatory genes were selected and are in the process of functional analyses. Several of these are genes represent unanticipated effectors of compound accumulation that could not be identified using traditional approaches. According to the original plan, the Cucurbit Genomics Network (http://www.icugi.org/), developed through an earlier BARD project (IS-3333-02), was expanded to serve as a public portal for the extensive metabolomics and transcriptomic data resulting from the current project. Importantly, this database was also expanded to include genomic and metabolomic resources of all the cucurbit crops, including genomes of cucumber and watermelon, EST collections, genetic maps, metabolite data and additional information. In addition, the database provides tools enabling researchers to identify genes, the expression patterns of which correlate with traits of interest. The project has significantly expanded the existing EST resource for melon and provides new molecular tools for marker-assisted selection. This information will be opened to the public by the end of 2013, upon the first publication describing the transcriptomic and metabolomics resources developed through the project. In addition, well-characterized RI lines are available to enable targeted breeding for genes of interest. Segregation of the RI lines for specific metabolites of interest has been shown, demonstrating the utility in these lines and our new molecular and metabolic data as a basis for selection targeting specific flavor, quality, nutritional and/or defensive compounds. To summarize, all the specific goals of the project have been achieved and in many cases exceeded. Large scale trascriptomic and metabolomic resources have been developed for melon and will soon become available to the community. The usefulness of these has been validated. A number of novel genes involved in fruit ripening have been selected and are currently being functionally analyzed. We thus fully addressed our obligations to the project. In our view, however, the potential value of the project outcomes as ultimately manifested may be far greater than originally anticipated. The resources developed and expanded under this project, and the tools created for using them will enable us, and others, to continue to employ resulting data and discoveries in future studies with benefits both in basic and applied agricultural - scientific research.
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Eshed, Yuval, i Sarah Hake. Exploring General and Specific Regulators of Phase Transitions for Crop Improvement. United States Department of Agriculture, listopad 2012. http://dx.doi.org/10.32747/2012.7699851.bard.

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The transition of plants from a juvenile to adult growth phase entails a wide range of changes in growth habit, physiological competence and composition. Strikingly, most of these changes are coordinated by the expression of a single regulator, micro RNA 156 (miR156) that coordinately regulates a family of SBP genes containing a miR156 recognition site in the coding region or in their 3’ UTR. In the framework of this research, we have taken a broad taxonomic approach to examine the role of miR156 and other genetic regulators in phase change transition and its implication to plant development and crop improvement. We set to: Determine the common and unique factors that are altered upon juvenile to adult phase transition. Determine the functions of select miR156 target genes in tomato and maize, and identify those targets that mediate phase transition. Characterize the role of miR172 and its targets in tomato phase change. Determine the relationships between the various molecular circuits directing phase change. Determine the effects of regulated manipulation of phase change genes on plant architecture and if applicable, productivity. In the course of the study, a new technology for gene expression was introduced – next generation sequencing (NGS). Hence some of the original experiments that were planned with other platforms of RNA profiling, primarily Affymetrix arrays, were substituted with the new technology. Yet, not all were fully completed. Moreover, once the initial stage was completed, each group chose to focus its efforts on specific components of the phase change program. The Israeli group focused on the roles of the DELAYED SYMPODIAL TERMINATION and FALSIFLORA factors in tomato age dependent programs whereas the US group characterized in detail the role of miR156 (also termed Cg) in other grasses and in maize, its interplay with the many genes encoding miR172.
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