Relevant bibliographies by topics / Phenotype Microarray

Academic literature on the topic 'Phenotype Microarray'

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Published: 10 March 2023

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Journal articles on the topic "Phenotype Microarray"

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De, Supriyo, Yongqing Zhang, John R. Garner, S. Alex Wang, and Kevin G. Becker. "Disease and phenotype gene set analysis of disease-based gene expression in mouse and human." Physiological Genomics 42A, no. 2 (October 2010): 162–67. http://dx.doi.org/10.1152/physiolgenomics.00008.2010.

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The genetic contributions to common disease and complex disease phenotypes are pleiotropic, multifactorial, and combinatorial. Gene set analysis is a computational approach used in the analysis of microarray data to rapidly query gene combinations and multifactorial processes. Here we use novel gene sets based on population-based human genetic associations in common human disease or experimental genetic mouse models to analyze disease-related microarray studies. We developed a web-based analysis tool that uses these novel disease- and phenotype-related gene sets to analyze microarray-based gene expression data. These gene sets show disease and phenotype specificity in a species-specific and cross-species fashion. In this way, we integrate population-based common human disease genetics, mouse genetically determined phenotypes, and disease or phenotype structured ontologies, with gene expression studies relevant to human disease. This may aid in the translation of large-scale high-throughput datasets into the context of clinically relevant disease phenotypes.
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Xuan, Jianhua. "Cross phenotype normalization of microarray data." Frontiers in Bioscience E2, no. 1 (2010): 171–86. http://dx.doi.org/10.2741/e80.

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Bochner, Barry, Vanessa Gomez, Michael Ziman, Shihui Yang, and Steven D. Brown. "Phenotype MicroArray Profiling of Zymomonas mobilis ZM4." Applied Biochemistry and Biotechnology 161, no. 1-8 (December 12, 2009): 116–23. http://dx.doi.org/10.1007/s12010-009-8842-2.

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von Eiff, Christof, Peter McNamara, Karsten Becker, Donna Bates, Xiang-He Lei, Michael Ziman, Barry R. Bochner, Georg Peters, and Richard A. Proctor. "Phenotype Microarray Profiling of Staphylococcus aureus menD and hemB Mutants with the Small-Colony-Variant Phenotype." Journal of Bacteriology 188, no. 2 (January 15, 2006): 687–93. http://dx.doi.org/10.1128/jb.188.2.687-693.2006.

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ABSTRACT Standard biochemical tests have revealed that hemin and menadione auxotrophic Staphylococcus aureus small-colony variants (SCVs) exhibit multiple phenotypic changes. To provide a more complete analysis of the SCV phenotype, two genetically defined mutants with a stable SCV phenotype were comprehensively tested. These mutants, generated via mutations in menD or hemB that yielded menadione and hemin auxotrophs, were subjected to phenotype microarray (PM) analysis of over 1,500 phenotypes (including utilization of different carbon, nitrogen, phosphate, and sulfur sources; growth stimulation or inhibition by amino acids and other nutrients, osmolytes, and metabolic inhibitors; and susceptibility to antibiotics). Compared to parent strain COL, the hemB mutant was defective in utilization of a variety of carbon sources, including Krebs cycle intermediates and compounds that ultimately generate ATP via electron transport. The phenotype of the menD mutant was similar to that of the hemB mutant, but the defects in carbon metabolism were more pronounced than those seen with the hemB mutant. In both mutant strains, hexose phosphates and other carbohydrates that provide ATP in the absence of electron transport stimulated growth. Other phenotypes of SCV mutants, such as hypersensitivity to sodium selenite, sodium tellurite, and sodium nitrite, were also uncovered by the PM analysis. Key results of the PM analysis were confirmed in independent growth studies and by using Etest strips for susceptibility testing. PM technology is a new and efficient technology for assessing cellular phenotypes in S. aureus.
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Card, Roderick, Jiancheng Zhang, Priya Das, Charlotte Cook, Neil Woodford, and Muna F. Anjum. "Evaluation of an Expanded Microarray for Detecting Antibiotic Resistance Genes in a Broad Range of Gram-Negative Bacterial Pathogens." Antimicrobial Agents and Chemotherapy 57, no. 1 (November 5, 2012): 458–65. http://dx.doi.org/10.1128/aac.01223-12.

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ABSTRACTA microarray capable of detecting genes for resistance to 75 clinically relevant antibiotics encompassing 19 different antimicrobial classes was tested on 132 Gram-negative bacteria. Microarray-positive results correlated >91% with antimicrobial resistance phenotypes, assessed using British Society for Antimicrobial Chemotherapy clinical breakpoints; the overall test specificity was >83%. Microarray-positive results without a corresponding resistance phenotype matched 94% with PCR results, indicating accurate detection of genes present in the respective bacteria by microarray when expression was low or absent and, hence, undetectable by susceptibility testing. The low sensitivity and negative predictive values of the microarray results for identifying resistance to some antimicrobial resistance classes are likely due to the limited number of resistance genes present on the current microarray for those antimicrobial agents or to mutation-based resistance mechanisms. With regular updates, this microarray can be used for clinical diagnostics to help accurate therapeutic options to be taken following infection with multiple-antibiotic-resistant Gram-negative bacteria and prevent treatment failure.
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Viti, Carlo, Enrico Tatti, and Luciana Giovannetti. "Phenotype MicroArray analysis of cells: fulfilling the promise." Research in Microbiology 167, no. 9-10 (November 2016): 707–9. http://dx.doi.org/10.1016/j.resmic.2016.08.003.

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TOHSATO, YUKAKO, TOMOYA BABA, YUSAKU MAZAKI, MASAHIRO ITO, BARRY L. WANNER, and HIROTADA MORI. "ENVIRONMENTAL DEPENDENCY OF GENE KNOCKOUTS ON PHENOTYPE MICROARRAY ANALYSIS IN ESCHERICHIA COLI." Journal of Bioinformatics and Computational Biology 08, supp01 (December 2010): 83–99. http://dx.doi.org/10.1142/s021972001000521x.

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Systematic studies have revealed that single gene deletions often display little phenotypic effects under laboratory conditions and that in many cases gene dispensability depends on the experimental conditions. To elucidate the environmental dependency of genes, we analyzed the effects of gene deletions by Phenotype MicroArray™ (PM), a system for quantitative screening of thousands of phenotypes in a high-throughput manner. Here, we proposed a new statistical approach to minimize error inherent in measurements of low respiration rates and find which mutants showed significant phenotypic changes in comparison to the wild-type. We show analyzing results from comprehensive PM assays of 298 single-gene knockout mutants in the Keio collection and two additional mutants under 1,920 different conditions. We focused on isozymes of these genes as simple duplications and analyzed correlations between phenotype changes and protein expression levels. Our results revealed divergence of the environmental dependency of the gene among the knockout genes and have also given some insights into possibilities of alternative pathways and availabilities of information on protein synthesis patterns to classify or predict functions of target genes from systematic phenotype screening.
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Çebi, Alper Han, and Şule Altıner. "Application of Chromosome Microarray Analysis in the Investigation of Developmental Disabilities and Congenital Anomalies: Single Center Experience and Review of NRXN3 and NEDD4L Deletions." Molecular Syndromology 11, no. 4 (2020): 197–206. http://dx.doi.org/10.1159/000509645.

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Chromosomal microarray analysis (CMA) is a first step test used for the diagnosis of patients with developmental delay, intellectual disability, autistic spectrum disorder, and multiple congenital anomalies. Its widespread usage has allowed genome-wide identification of copy number variations (CNVs). In our study, we performed a retrospective study on clinical and microarray data of 237 patients with developmental disabilities and/or multiple congenital anomalies and investigated the clinical utility of CMA. Phenotype-associated CNVs were detected in 15.18% of patients. Besides, we detected submicroscopic losses on 14q24.3q31.1 in a patient with speech delay and on 18q21.31q21.32 in twin patients with seizures. Deletions of <i>NRXN3</i> and <i>NEDD4L</i> were responsible for the phenotypes, respectively. This study showed that CMA is a powerful diagnostic tool in this patient group and expands the genotype-phenotype correlations on developmental disabilities.
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Gerstgrasser, Matthias, Sarah Nicholls, Michael Stout, Katherine Smart, Chris Powell, Theodore Kypraios, and Dov Stekel. "A Bayesian approach to analyzing phenotype microarray data enables estimation of microbial growth parameters." Journal of Bioinformatics and Computational Biology 14, no. 03 (June 2016): 1650007. http://dx.doi.org/10.1142/s0219720016500074.

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Biolog phenotype microarrays (PMs) enable simultaneous, high throughput analysis of cell cultures in different environments. The output is high-density time-course data showing redox curves (approximating growth) for each experimental condition. The software provided with the Omnilog incubator/reader summarizes each time-course as a single datum, so most of the information is not used. However, the time courses can be extremely varied and often contain detailed qualitative (shape of curve) and quantitative (values of parameters) information. We present a novel, Bayesian approach to estimating parameters from Phenotype Microarray data, fitting growth models using Markov Chain Monte Carlo (MCMC) methods to enable high throughput estimation of important information, including length of lag phase, maximal “growth” rate and maximum output. We find that the Baranyi model for microbial growth is useful for fitting Biolog data. Moreover, we introduce a new growth model that allows for diauxic growth with a lag phase, which is particularly useful where Phenotype Microarrays have been applied to cells grown in complex mixtures of substrates, for example in industrial or biotechnological applications, such as worts in brewing. Our approach provides more useful information from Biolog data than existing, competing methods, and allows for valuable comparisons between data series and across different models.
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Holt, S., and E. Sweeney. "Using microarray to diagnose Noonan Syndrome and predict phenotype." Archives of Disease in Childhood 97, Suppl 1 (May 2012): A15.3—A16. http://dx.doi.org/10.1136/archdischild-2012-301885.38.

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Dissertations / Theses on the topic "Phenotype Microarray"

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Wennmalm, Kristian. "Analytical strategies for identifying relevant phenotypes in microarray data /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-401-3/.

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Sjödin, Andreas. "Populus transcriptomics : from noise to biology /." Umeå : Department of Plant Physiology, Umeå University, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1423.

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Mok, Bobo. "Genomic and transcriptomic variation in blood stage Plasmodium falciparum /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-291-0/.

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Martínez, Enguita David. "Identification of personalized multi-omic disease modules in asthma." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-15987.

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Asthma is a respiratory syndrome associated with airflow limitation, bronchial hyperresponsiveness and inflammation of the airways in the lungs. Despite the ongoing research efforts, the outstanding heterogeneity displayed by the multiple forms in which this condition presents often hampers the attempts to determine and classify the phenotypic and endotypic biological structures at play, even when considering a limited assembly of asthmatic subjects. To increase our understanding of the molecular mechanisms and functional pathways that govern asthma from a systems medicine perspective, a computational workflow focused on the identification of personalized transcriptomic modules from the U-BIOPRED study cohorts, by the use of the novel MODifieR integrated R package, was designed and applied. A feature selection of candidate asthma biomarkers was implemented, accompanied by the detection of differentially expressed genes across sample categories, the production of patient-specific gene modules and the subsequent construction of a set of core disease modules of asthma, which were validated with genomic data and analyzed for pathway and disease enrichment. The results indicate that the approach utilized is able to reveal the presence of components and signaling routes known to be crucially involved in asthma pathogenesis, while simultaneously uncovering candidate genes closely linked to the latter. The present project establishes a valuable pipeline for the module-driven study of asthma and other related conditions, which can provide new potential targets for therapeutic intervention and contribute to the development of individualized treatment strategies.
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Rösel, Anja [Verfasser], and Frank [Akademischer Betreuer] Pessler. "Application of the Biolog Phenotype MicroArray TM to study changes in host cell metabolism during influenza A virus infection / Anja Rösel ; Akademischer Betreuer: Frank Peßler ; Institut für Experimentelle Infektionsforschung des Twincore Zentrum für Experimentelle und Klinische Infektionsforschung." Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2017. http://nbn-resolving.de/urn:nbn:de:gbv:354-2017061613.

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Rösel, Anja [Verfasser], and Frank [Akademischer Betreuer] Peßler. "Application of the Biolog Phenotype MicroArray TM to study changes in host cell metabolism during influenza A virus infection / Anja Rösel ; Akademischer Betreuer: Frank Peßler ; Institut für Experimentelle Infektionsforschung des Twincore Zentrum für Experimentelle und Klinische Infektionsforschung." Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2017. http://d-nb.info/1135490783/34.

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Turton, Nicola. "Association of gene expression and genomic change, analysed using microarrays, with phenotype in breast carcinoma." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/30770.

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Breast cancer is the commonest malignancy to affect women and approximately 1 in 9 women (12 %) will develop the disease in developed countries (Burstein and Winer 2000). A major problem for treatment is the development of a drug resistant phenotype, whereby the tumour fails to respond to chemotherapy. This phenotype arises from altered gene expression in the resistant cells, which can occur by changes in transcription and/or genomic alteration. Other phenotypic properties of breast carcinoma cells may also arise in this way, and gene expression profiles can be linked to different breast tumour phenotypes, such as oestrogen receptor (ER) status, clinical tumour stage and tumour size (Martin et al., 2000). In this thesis cDNA microarrays were utilised to study both genomic amplification and RNA expression changes occurring in human breast carcinoma. These changes were related to phenotypic characteristics including a doxorubicin (Dox) resistant phenotype, hormone receptor status, tumour grade and type. Several gene clusters involving the development of resistance and the eventual Dox resistant phenotype in breast cancer cell lines were elucidated, associated with both these was the multi drug resistance 1 gene (ABCB1). Potential therapeutic targets in these cells e.g. the oxytocin receptor gene (OXTR) were also indicated. Regions of genomic amplification and specific genes were elucidated some of these have previously been described while others are novel. Some of the genomic changes were associated with tumour phenotype, for example gene amplification at chromosome 2p25 and 22qll were specific to lymph node positive tumours and 2 genes were consistently found amplified in these regions, LPIN1 and DGSI respectively. The findings of this study have contributed to the general understanding of genetic events occurring in breast cancer and associations between these changes and phenotype were suggested.
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Yahaya, Badrul H. "Analysis of time-dependent transcriptomic and phenotypic changes associated with repair and regeneration in the airway epithelium." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4800.

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The airway epithelium demonstates the ability to quickly repair following physical injury. The morphologic features of this dynamic repair process have been well characterised at the anatomic and cellular level using a number of animal model systems and these studies have provided a solid foundation upon which our understanding of normal repair is build. With the advent of molecular and bioinformatic tools and resources the opportunity exists to extend the value of these models in defining the molecular pathways and interactions that underlay the normal repair process. This thesis represents a realisation of this opportunity. A large animal model was developed in which selected areas of airway epithelium were subjected to bronchial brush biopsy as part of routine bronchoscopic examination prcedures in anaethetised sheep. The process resulted in a physical perturbation of the normal pseudostratified structure of the sheep airwway epithelium at specific locations. By careful experimental design it was possible, within the same animals. to identify and sample from sites undergoing repair at different intervals subsequent in injury. To supplement the histological evaluation of the repair process and align findings with extablished small animal models of airway epithelial repair proliferative cell labelling strategies were implemented in order to study the location and extent of cellular proliferation occurring duringthe repair process. Molecular approaches towards defining the transcriptional response to physical injury comprised application of microarray technology using a commercially sources array platform. Such approach demanted preliminary effort directed towards optimising RNA integrity and yield from airway samples. Following preliminary studies directed towards optimising the model conditions patterns of airway epithelial repair following bronchial brush biopsy were studies in eight sheep at degined time points (6 hours, 1,3, & 7 days) post-injury. Bronchial brush biopsy resulted in the acute removal of the epithelial cell layer and components of the underlying structures. repair processes were rapidly implemented through initial epithelial dedifferentiation, proliferatino and migration at the wound margins and subsequent time-depentend changes in the proportion of subepithelial structures, including smooth muscle and blood vessels, as the epithelial surface moved towards repair. Transcriptional analysis revewaled that over 13,000 probes showed evidence of differential expession at some point during the repair process (p<0.05), whilst of these, 1491 probes had in excess of a two-fold change in expression. array results were validated against conventional semi-quantitative RT-PCR for selected genes. Differentially expressed genes with previously characterised roles in epithelial migration, prolifereation and differentiation were identified during the repair process. The relative emphasis of gene products with particular functional roles varied during the course of repair. Indeed gene ontology (GO) terms identified included those associated with the inflammatory response, cellular migration, extracellular matrix activities, differentiation, proliferation, cellular development, cell cycle activities, cellular adhesion, apoptosis and mitosis. In addition the Kyoto Encyclopedia of Genes and Gneomes (KEGG) databases were queried and such process indicated the involvement of cell communication, 053 and complement and coagulation cascade pathways throughout the repair process, initial (6h) Toll-like receptor and cytokine-cytoine receptor interaction pathways, and the progressive involement of cell cycle, focal adhesion and extracellulaar matrix (ECM)-receptor, and cytokine interaction pathways as the epithelium repaired. The model of airway epithelial injury developed in this thesis generated features broadly consistent with those previosly described in relation to various small animal model systems. Importantly, and in addition, this thesis defines the molecular features associated with repair in this model system and provides a useful resource with which to assess the comparative fetures of the airway transcriptional response to physical injury, It is through such comparison, using analogous methodology, that the fundamental pathways and interactions that underlay normal repair and regeneration can be identified and therafter extended towards inderstanding the basis for variation associated with natural and experimental disease.
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Shaffer, Justin P., Jana M. U'Ren, Rachel E. Gallery, David A. Baltrus, and A. Elizabeth Arnold. "An Endohyphal Bacterium (Chitinophaga, Bacteroidetes) Alters Carbon Source Use by Fusarium keratoplasticum (F. solani Species Complex, Nectriaceae)." FRONTIERS MEDIA SA, 2017. http://hdl.handle.net/10150/623193.

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Bacterial endosymbionts occur in diverse fungi, including members of many lineages of Ascomycota that inhabit living plants. These endosymbiotic bacteria (endohyphal bacteria, EHB) often can be removed from living fungi by antibiotic treatment, providing an opportunity to assess their effects on functional traits of their fungal hosts. We examined the effects of an endohyphal bacterium (Chitinophaga sp., Bacteroidetes) on substrate use by its host, a seed-associated strain of the fungus Fusarium keratoplasticum, by comparing growth between naturally infected and cured fungal strains across 95 carbon sources with a Biolog((R)) phenotypic microarray. Across the majority of substrates (62%), the strain harboring the bacterium significantly outperformed the cured strain as measured by respiration and hyphal density. These substrates included many that are important for plant-and seed fungus interactions, such as D-trehalose, myoinositol, and sucrose, highlighting the potential influence of EHB on the breadth and efficiency of substrate use by an important Fusariurn species. Cases in which the cured strain outperformed the strain harboring the bacterium were observed in only 5% of substrates. We propose that additive or synergistic substrate use by the fungus bacterium pair enhances fungal growth in this association. More generally, alteration of the breadth or efficiency of substrate use by dispensable EHB may change fungal niches in short timeframes, potentially shaping fungal ecology and the outcomes of fungal-host interactions.
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Roberge, Christopher (Christopher M. ). "Design, manufacture, and application of DNA microarrays to study gene expression phenotypes of lysine-producing Corynebacterium glutamicum." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/32322.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, 2005.
Includes bibliographical references (leaves 197-213).
Corynebacterium glutamicum partial genome DNA microarrays were constructed that were capable of assaying the transcriptional profile of the genes of pathways involved in central carbon metabolism and lysine biosynthesis. It was found that to ensure arrays of high quality, protocols applying the arrays should include DNase treatment of RNA samples. additional RNA filtration purification steps, and the use of gene specific primers in the formation of labeled cDNA through reverse transcription. After implementing these procedures, the accuracy and reproducibility of the array data were validated. The microarrays were used to explore the effects of the over-expression of the key anaplerotic enzyme pyruvate carboxylase and the use of different medium carbon source compositions, both of which have been shown to influence the yields of biomass on carbon and of lysine on biomass. Three different strains of C. glutamicum that were grown on six different minimal medium formulations that varied in their balance of glucose and lactate were assayed by isolating total mRNA samples from cultures in three different phases of growth and lysine production. Genes associated with glycolysis and the pentose phosphate pathway showed decreased transcript concentrations as the available carbon source was shifted from glucose to lactate, while those associated with the TCA cycle and the glyoxylate bypass demonstrated increased transcription. As the cultures stopped generating biomass and began generating lysine, mRNA of genes associated with lysine synthesis and export was measured at elevated concentrations.
(cont.) Reduced gene expression trends seen for aspartokinase and aspartate semialdehyde dehydrogenase suggest that the enzymes are bottlenecks to lysine production, particularly when pyruvate carboxylase is over-expressed and lactate is the available carbon source. This over-expressing strain also had higher transcription levels of the genes of biotin synthesis. and lower transcription levels of the acyl-coA carboxylases dtsRl, dtsR2, accC, and accD. Other results implied that malic enzyme is co-expressed with pyruvate carboxylase to better allow cultures grown on lactate to produce NADPH in the absence of significant pentose phosphate pathway flux. Also, the transcriptional and flux profiles of a pair of C. glutamicum strains grown on two different medium compositions of isotopically labeled glucose and lactate were determined simultaneously from the same set of actively growing and lysine-producing cultures. Flux maps for each of the four combinations of strain and medium were constructed using calculations derived from metabolite balances and GC-MS measurements of the isotopic distributions within biomass hydrolysates of the pseudo-steady-state cultures. Comparisons of the two sets of data showed that 19 of 28 pairs of flux and transcription measurements had trends with good agreement with one another. Different pathways of the metabolic network were found to be controlled via transcription in varying degrees. On average, the Embden- Meyerhof-Parnas pathway was shown to be less likely to be regulated though transcription than the pathways of the tricarboxylic acid cycle and central carbon anaplerosis.
(cont.) In the split pathway available to the cells for producing lysine, the succinylation branch showed an increase in flux for only the case of a pyruvate carboxylase over-expressing strain that was grown on lactate, while the alternate dehydrogenation branch showed a complementary decrease in flux. These flux changes were matched by changes in transcription that only occurred for the same culture and growth medium. Through these findings we have demonstrated the application of C. glutamicum DNA microarrays to the determination of how the cells regulate their responses at the transcriptional level to changes in both gene over-expression and medium composition.
by Christopher Roberge.
Ph.D.
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Book chapters on the topic "Phenotype Microarray"

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Shea, April, Mark Wolcott, Simon Daefler, and David A. Rozak. "Biolog Phenotype Microarrays." In Microbial Systems Biology, 331–73. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-827-6_12.

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Mackie, Amanda M., Karl A. Hassan, Ian T. Paulsen, and Sasha G. Tetu. "Biolog Phenotype MicroArrays for Phenotypic Characterization of Microbial Cells." In Methods in Molecular Biology, 123–30. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-712-9_10.

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Bochner, Barry R. "Phenomics and Phenotype Microarrays: Applications Complementing Metagenomics." In Handbook of Molecular Microbial Ecology I, 533–40. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118010518.ch59.

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Gawand, Pratish, Laurence Yang, William R. Cluett, and Radhakrishnan Mahadevan. "Metabolic Model Refinement Using Phenotypic Microarray Data." In Methods in Molecular Biology, 47–59. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-299-5_3.

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Thorn, Christopher C., Deborah Williams, and Thomas C. Freeman. "Oligonucleotide Microarray Expression Profiling of Contrasting Invasive Phenotypes in Colorectal Cancer." In Methods in Molecular Biology, 203–21. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-163-5_17.

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Perez, Dragana Veljkovic, and Kay A. Robbins. "Detection of Phenotypes in Microarray Data Using Force- Directed Placement Transformss." In Machine Learning and Data Mining in Pattern Recognition, 320–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-23199-5_24.

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Baarda, Benjamin I., and Aleksandra E. Sikora. "Phenotypic MicroArray Screening of Neisseria gonorrhoeae in Chemically Defined Liquid Medium." In Neisseria gonorrhoeae, 207–16. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9496-0_13.

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Fox, Edward M., and Kieran Jordan. "High-Throughput Characterization of Listeria monocytogenes Using the OmniLog Phenotypic Microarray." In Methods in Molecular Biology, 103–8. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0703-8_9.

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Luque-Sastre, Laura, Kieran Jordan, Séamus Fanning, and Edward M. Fox. "High-Throughput Characterization of Listeria monocytogenes Using the OmniLog Phenotypic Microarray." In Listeria Monocytogenes, 107–13. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0982-8_8.

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Chua, Gordon. "Identification of Transcription Factor Targets by Phenotypic Activation and Microarray Expression Profiling in Yeast." In Methods in Molecular Biology, 19–35. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-540-4_2.

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Conference papers on the topic "Phenotype Microarray"

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Jacobsen, Janet S., Dominique C. Joyner, and Sharon E. Borglin. "Visualization of Growth Curve Data from Phenotype Microarray Experiments." In 2007 11th International Conference Information Visualization (IV '07). IEEE, 2007. http://dx.doi.org/10.1109/iv.2007.131.

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Tohsato, Yukako, Tadahiro Taniguchi, Hirotada Mori, and Masahiro Ito. "Analyzing Phenotype Microarray Data for Escherichia coli Using an Infinite Relational Model." In 2021 IEEE 9th International Conference on Bioinformatics and Computational Biology (ICBCB). IEEE, 2021. http://dx.doi.org/10.1109/icbcb52223.2021.9459236.

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Dymacek, Julian, and Nancy Lan Guo. "Systems Approach to Identifying Relevant Pathways from Phenotype Information in Dose-Dependent Time Series Microarray Data." In 2011 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2011. http://dx.doi.org/10.1109/bibm.2011.76.

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Misman, M. F., S. Deris, S. Z. M. Hashim, R. Jumali, and M. S. Mohamad. "Pathway-Based Microarray Analysis for Defining Statistical Significant Phenotype-Related Pathways: A Review of Common Approaches." In 2009 International Conference on Information Management and Engineering. IEEE, 2009. http://dx.doi.org/10.1109/icime.2009.103.

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Yeh, Hsiang-Yuan, Yi-Yu Liu, Cheng-Yu Yeh, and Von-Wun Soo. "Identifying Prostate Cancer-Related Networks from Microarray Data Based on Genotype-Phenotype Networks Using Markov Blanket Search." In 2010 IEEE International Conference on BioInformatics and BioEngineering. IEEE, 2010. http://dx.doi.org/10.1109/bibe.2010.64.

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Chen, Argon. "Analysis of microarray data with multiple phenotypes." In Industrial Engineering (CIE39). IEEE, 2009. http://dx.doi.org/10.1109/iccie.2009.5223511.

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Zhao, Yuhai, Ying Yin, and Guoren Wang. "Unsupervised Identifying Diagnostic Genes and Specific Phenotypes from Microarray Data." In 2006 International Conference on Computational Intelligence and Security. IEEE, 2006. http://dx.doi.org/10.1109/iccias.2006.294239.

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Hsun-Hsien Chang and M. McGeachie. "Phenotype prediction by integrative network analysis of SNP and gene expression microarrays." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091689.

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Bolger, Kenneth. "LSC Abstract – The use of microarray analysis of gene signalling to determine heterogeneity of COPD exacerbation phenotypes." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.yi5.

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Huang, Alice H., and Robert L. Mauck. "Repeated Dynamic Loading Modulates Cartilage Gene Expression but Does Not Improve Mechanical Properties of MSC-Laden Hydrogels." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204339.

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Mesenchymal stem cells (MSCs) are a multi-potential cell type that can differentiate toward a variety of tissue-specific phenotypes, including cartilage. Given their chondrogenic potential, MSCs are a promising cell source for cartilage tissue engineering (TE). However, while MSCs readily undergo chondrogenesis in 3D culture and deposit a cartilage-like matrix, the mechanical properties of MSC-seeded constructs are greatly inferior to chondrocyte-seeded constructs similarly maintained [1]. To date, optimization strategies for enhancing functional MSC chondrogenesis, including increasing seeding density and transient application of growth factor, have shown limited success [3]. Using microarray analysis, we have recently demonstrated that mis-expression of certain genes, including lubricin, chondromodulin and RGD-CAP, a collagen associated protein, may underlie this disparity in mechanical function [2]. In this study, we examined dynamic compression as an alternative method to enhance MSC differentiation. Previous work using chondrocyte-based constructs have demonstrated that matrix biosynthesis and mechanical properties were improved with the application of cyclic compression [4]. Furthermore, upregulation of lubricin was observed when surface motion was applied to chondrocyte-seeded porous scaffolds [5]. While significant effort has gone toward optimizing loading parameters to direct tissue growth of chondrocyte-based constructs, few studies have examined the effects of mechanical stimulation on MSC-based constructs. Some have demonstrated positive effects on MSC chondrogenesis with application of compressive loading [6, 7], while others have shown that long-term loading may adversely affect the developing mechanical properties of MSC-seeded constructs [8]. In this study, we examined the effects of repeated dynamic compressive loading on MSC chondrogenesis and showed that mechanical properties and gene expression were modulated by this loading modality.
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Reports on the topic "Phenotype Microarray"

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Tucker, Mark L., Shimon Meir, Amnon Lers, Sonia Philosoph-Hadas, and Cai-Zhong Jiang. Elucidation of signaling pathways that regulate ethylene-induced leaf and flower abscission of agriculturally important plants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597929.bard.

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The Problem: Abscission is a highly regulated process, occurring as a natural terminal stage of development, in which various organs are separated from the parent plant. In most plant species, the process is initiated by a decrease in active auxin in the abscission zone (AZ) and an increase in ethylene, and may be accelerated by postharvest or environmental stresses. Another potential key regulator in abscission is IDA (Inflorescence Deficient in Abscission), which was identified as an essential peptide signal for floral organ abscission in Arabidopsis. However, information is still lacking regarding the molecular mechanisms integrating all these regulators. In our previous BARD funded research we made substantial progress towards understanding these molecular events in tomato, and the study is still in progress. We established a powerful platform for analysis of genes for regulatory proteins expressed in AZ. We identified changes in gene expression for several transcription factors (TFs) directly linked to ethylene and auxin signaling and several additional regulatory proteins not so obviously linked to these hormones. Moreover, we demonstrated using a virus-induced gene silencing (VIGS) assay that several play a functional role in the onset of abscission. Based on these results we have selected 14 genes for further analysis in stably transformed tomato plants. All 14 genes were suppressed by RNA interference (RNAi) using a constitutive promoter, and 5 of them were also suppressed using an abscission-specific promoter. Transformations are currently at different stages of progress including some lines that already display an abscission phenotype. Objectives: We propose here to (1) complete the functional analysis of the stably transformed tomato plants with T2 lines and perform transcriptome analysis using custom abscission-specific microarrays; (2) conduct an indepth analysis of the role of IDA signaling in tomato leaf and flower abscission; (3) perform transcriptome and proteome analyses to extend the earlier gene expression studies to identify transcripts and proteins that are highly specific to the separation layer (i.e., target cells for cell separation) prior to the onset of abscission; (4) extend and compliment the work in tomato using a winnowed set of genes in soybean. Methodology: Next Generation Sequencing (NGS) of mRNA will be used to further increase the list of abscission-associated genes, and for preparation of a custom tomato abscission microarray to test altered gene expression in transgenic plants. Tandem mass spectrometry (LC-MS/MS) of protein extracts from leaf petiole, flower pedicel and their AZ tissues will be used to identify the proteome of the AZ before and during abscission. AZ-specific gene promoters will be used in stably transformed tomato plants to reduce non-target phenotypes. The bean pod mottle virus (BPMV) plasmid vectors will be used for VIGS analysis in soybean. Expected Contribution: Our study will provide new insights into the regulation of ethylene-induced abscission by further revealing the role of key regulators in the process. This will permit development of novel techniques for manipulating leaf and flower abscission, thereby improving the postharvest performance of agriculturally important crops.
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Joyner, Dominique, Julian Fortney, Romy Chakraborty, and Terry Hazen. Adaptation of the Biolog Phenotype MicroArrayTM Technology to Profile the Obligate Anaerobe Geobacter metallireducens. Office of Scientific and Technical Information (OSTI), May 2010. http://dx.doi.org/10.2172/985923.

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Meir, Shimon, Michael S. Reid, Cai-Zhong Jiang, Amnon Lers, and Sonia Philosoph-Hadas. Molecular Studies of Postharvest Leaf and Flower Senescence. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592657.bard.

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Original objectives: To understand the regulation of abscission by exploring the nature of changes of auxin-related gene expression in tomato (Lycopersicon esculatumMill) abscission zones (AZs) following organ removal, and by analyzing the function of these genes. Our specific goals were: 1) To complete the microarray analyses in tomato flower and leaf AZs, for identifying genes whose expression changes early in response to auxin depletion; 2) To examine, using virus-induced gene silencing (VIGS), the effect of silencing target genes on ethylene sensitivity and abscission competence of the leaf and flower AZs; 3) To isolate and characterize promoters from AZ-specific genes to be used in functional analysis; 4) To generate stable transgenic tomato plants with selected genes silenced with RNAi, under the control of an AZ-specific promoter, for further characterization of their abscission phenotypes. Background: Abscission, the separation of organs from the parent plant, results in postharvest quality loss in many ornamentals and other fresh produce. The process is initiated by changes in the auxin gradient across the AZ, and is triggered by ethylene. Although changes in gene expression have been correlated with the ethylene-mediated execution of abscission, there is almost no information on the initiation of the abscission process, as the AZ becomes sensitized to ethylene. The present project was focused on elucidating these early molecular regulatory events, in order to gain a better control of the abscission process for agricultural manipulations. Major conclusions, solutions, achievements: Microarray analyses, using the Affymetrix Tomato GeneChip®, revealed changes in expression, occurring early in abscission, of many genes with possible regulatory functions. These included a range of auxin- and ethylene-related transcription factors (TFs), other TFs that are transiently induced just after flower removal, and a set of novel AZ-specific genes. We also identified four different defense-related genes, including: Cysteine-type endopeptidase, α- DOX1, WIN2, and SDF2, that are newly-associated with the late stage of the abscission process. This supports the activation of different defense responses and strategies at the late abscission stages, which may enable efficient protection of the exposed tissue toward different environmental stresses. To facilitate functional studies we implemented an efficient VIGS system in tomato, and isolated two abscission-specific promoters (pTAPG1 and pTAPG4) for gene silencing in stable transformation. Using the VIGS system we could demonstrate the importance of TAPGs in abscission of tomato leaf petioles, and evaluated the importance of more than 45 genes in abscission. Among them we identified few critical genes involved in leaf and flower abscission. These included: PTRP-F1, PRP, TKN4, KNOTTED-like homeobox TF, KD1, and KNOX-like homeodomain protein genes, the silencing of which caused a striking retardation of pedicel abscission, and ERF1, ERF4, Clavata-like3 protein, Sucrose transporter protein, and IAA10 genes, the silencing of which delayed petiole abscission. The importance of PRPand KD1 genes in abscission was confirmed also by antisense–silencing using pTAPG4. Experiments testing the effects of RNAi silencing of few other genes are still in progress, The analysis of the microarray results of flower and leaf AZs allowed us to establish a clear sequence of events occurring during acquisition of tissue sensitivity to ethylene, and to confirm our hypothesis that acquisition of ethylene sensitivity in the AZ is associated with altered expression of auxin-regulated genes in both AZs. Implication, both scientific and agricultural: Our studies had provided new insights into the regulation of the abscission process, and shaded light on the molecular mechanisms that drive the acquisition of abscission competence in the AZ. We pointed out some critical genes involved in regulation of abscission, and further expanded our knowledge of auxin-ethylene cross talk during the abscission process. This permits the development of novel techniques for manipulating abscission, and thereby improving the postharvest performance of ornamentals and other crops.
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Lers, Amnon, and Gan Susheng. Study of the regulatory mechanism involved in dark-induced Postharvest leaf senescence. United States Department of Agriculture, January 2009. http://dx.doi.org/10.32747/2009.7591734.bard.

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Postharvest leaf senescence contributes to quality losses in flowers and leafy vegetables. The general goal of this research project was to investigate the regulatory mechanisms involved in dark-induced leaf senescence. The regulatory system involved in senescence induction and control is highly complex and possibly involves a network of senescence promoting pathways responsible for activation of the senescence-associated genes. Pathways involving different internal signals and environmental factors may have distinctive importance in different leaf senescence systems. Darkness is known to have a role in enhancement of postharvest leaf senescence and for getting an insight into its regulatory mechanism/s we have applied molecular genetics and functional genomics approaches. The original objectives were: 1. Identification of dark-induced SAGs in Arabidopsis using enhancer/promoter trap lines and microarray approaches; 2. Molecular and functional characterization of the identified genes by analyzing their expression and examining the phenotypes in related knockout mutant plants; 3. Initial studies of promoter sequences for selected early dark-induced SAGs. Since genomic studies of senescence, with emphasis on dark-induced senescence, were early-on published which included information on potential regulatory genes we decided to use this new information. This is instead of using the uncharacterized enhancer/promoter trap lines as originally planned. We have also focused on specific relevant genes identified in the two laboratories. Based on the available genomic analyses of leaf senescence 10 candidate genes hypothesized to have a regulatory role in dark-induced senescence were subjected to both expression as well as functional analyses. For most of these genes senescence-specific regulation was confirmed, however, functional analyses using knock-out mutants indicated no consequence to senescence progression. The transcription factor WARK75 was found to be specifically expressed during natural and dark-induced leaf senescence. Functional analysis demonstrated that in detached leaves senescence under darkness was significantly delayed while no phenotypic consequences could be observed on growth and development, including no effect on natural leaf senescence,. Thus, WARKY75 is suggested to have a role in dark-induced senescence, but not in natural senescence. Another regulatory gene identified to have a role in senescence is MKK9 encoding for a Mitogen-Activated Protein Kinase Kinase 9 which is upregulated during senescence in harvested leaves as well as in naturally senescing leaves. MKK9 can specifically phosphorylate another kinase, MPK6. Both knockouts of MKK9 and MPK6 displayed a significantly senescence delay in harvested leaves and possibly function as a phosphorelay that regulates senescence. To our knowledge, this is the first report that clearly demonstrates the involvement of a MAP kinase pathway in senescence. This research not only revealed a new signal transduction pathway, but more important provided significant insights into the regulatory mechanisms underlying senescence in harvested leaves. In an additional line of research we have employed the promoter of the senescence-induced BFN1 gene as a handle for identifying components of the regulatory mechanism. This gene was shown to be activated during darkinduced senescence of detached leaves, as well as natural senescence. This was shown by following protein accumulation and promoter activity which demonstrated that this promoter is activated during dark-induced senescence. Analysis of the promoter established that, at least some of the regulatory sequences reside in an 80 bps long fragment of the promoter. Overall, progress was made in identification of components with a role in dark-induced senescence in this project. Further studies should be done in order to better understand the function of these components and develop approaches for modulating the progress of senescence in crop plants for the benefit of agriculture.
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Barg, Rivka, Erich Grotewold, and Yechiam Salts. Regulation of Tomato Fruit Development by Interacting MYB Proteins. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7592647.bard.

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Background to the topic: Early tomato fruit development is executed via extensive cell divisions followed by cell expansion concomitantly with endoreduplication. The signals involved in activating the different modes of growth during fruit development are still inadequately understood. Addressing this developmental process, we identified SlFSM1 as a gene expressed specifically during the cell-division dependent stages of fruit development. SlFSM1 is the founder of a class of small plant specific proteins containing a divergent SANT/MYB domain (Barg et al 2005). Before initiating this project, we found that low ectopic over-expression (OEX) of SlFSM1 leads to a significant decrease in the final size of the cells in mature leaves and fruits, and the outer pericarp is substantially narrower, suggesting a role in determining cell size and shape. We also found the interacting partners of the Arabidopsis homologs of FSM1 (two, belonging to the same family), and cloned their tomato single homolog, which we named SlFSB1 (Fruit SANT/MYB–Binding1). SlFSB1 is a novel plant specific single MYB-like protein, which function was unknown. The present project aimed at elucidating the function and mode of action of these two single MYB proteins in regulating tomato fruit development. The specific objectives were: 1. Functional analysis of SlFSM1 and its interacting protein SlFSB1 in relation to fruit development. 2. Identification of the SlFSM1 and/or SlFSB1 cellular targets. The plan of work included: 1) Detailed phenotypic, histological and cellular analyses of plants ectopically expressing FSM1, and plants either ectopically over-expressing or silenced for FSB1. 2) Extensive SELEX analysis, which did not reveal any specific DNA target of SlFSM1 binding, hence the originally offered ChIP analysis was omitted. 3) Genome-wide transcriptional impact of gain- and loss- of SlFSM1 and SlFSB1 function by Affymetrix microarray analyses. This part is still in progress and therefore results are not reported, 4) Search for additional candidate partners of SlFSB1 revealed SlMYBI to be an alternative partner of FSB1, and 5) Study of the physical basis of the interaction between SlFSM1 and SlFSB1 and between FSB1 and MYBI. Major conclusions, solutions, achievements: We established that FSM1 negatively affects cell expansion, particularly of those cells with the highest potential to expand, such as the ones residing inner to the vascular bundles in the fruit pericarp. On the other hand, FSB1 which is expressed throughout fruit development acts as a positive regulator of cell expansion. It was also established that besides interacting with FSM1, FSB1 interacts also with the transcription factor MYBI, and that the formation of the FSB1-MYBI complex is competed by FSM1, which recognizes in FSB1 the same region as MYBI does. Based on these findings a model was developed explaining the role of this novel network of the three different MYB containing proteins FSM1/FSB1/MYBI in the control of tomato cell expansion, particularly during fruit development. In short, during early stages of fruit development (Phase II), the formation of the FSM1-FSB1 complex serves to restrict the expansion of the cells with the greatest expansion potential, those non-dividing cells residing in the inner mesocarp layers of the pericarp. Alternatively, during growth phase III, after transcription of FSM1 sharply declines, FSB1, possibly through complexing with the transcription factor MYBI serves as a positive regulator of the differential cell expansion which drives fruit enlargement during this phase. Additionally, a novel mechanism was revealed by which competing MYB-MYB interactions could participate in the control of gene expression. Implications, both scientific and agricultural: The demonstrated role of the FSM1/FSB1/MYBI complex in controlling differential cell growth in the developing tomato fruit highlights potential exploitations of these genes for improving fruit quality characteristics. Modulation of expression of these genes or their paralogs in other organs could serve to modify leaf and canopy architecture in various crops.
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