Relevant bibliographies by topics / Genome wide screening

Academic literature on the topic 'Genome wide screening'

Author: Grafiati

Published: 10 December 2022

Last updated: 10 March 2023

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Journal articles on the topic "Genome wide screening"

Tsuchihara, Katsuya. "Nation-wide genome screening data-base." Annals of Oncology 28 (October 2017): ix19. http://dx.doi.org/10.1093/annonc/mdx551.

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Kamath, R. "Genome-wide RNAi screening in Caenorhabditis elegans." Methods 30, no. 4 (August 2003): 313–21. http://dx.doi.org/10.1016/s1046-2023(03)00050-1.

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LaFlamme, Brooke. "A CRISPR method for genome-wide screening." Nature Genetics 46, no. 2 (January 29, 2014): 99. http://dx.doi.org/10.1038/ng.2887.

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Livak, Kenneth J., Jeffrey Marmaro, and John A. Todd. "Towards fully automated genome–wide polymorphism screening." Nature Genetics 9, no. 4 (April 1995): 341–42. http://dx.doi.org/10.1038/ng0495-341.

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Han, Chan-Hee, In-Hwan Song, and Si-Woong Lee. "Automatic Segmentation of Cellular Images for High-Throughput Genome-Wide RNA Interference Screening." Journal of the Korea Contents Association 10, no. 4 (April 28, 2010): 19–27. http://dx.doi.org/10.5392/jkca.2010.10.4.019.

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Shaffer, Catherine. "CRISPR's Rapid Rise Shakes Up Genome-Wide Screening." Genetic Engineering & Biotechnology News 41, no. 5 (May 1, 2021): 46–49. http://dx.doi.org/10.1089/gen.41.05.13.

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Yu, Jason S. L., and Kosuke Yusa. "Genome-wide CRISPR-Cas9 screening in mammalian cells." Methods 164-165 (July 2019): 29–35. http://dx.doi.org/10.1016/j.ymeth.2019.04.015.

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Lee, C. Y. Daniel, and X. William Yang. "Huntington's Disease: Genome-wide Neuroprotection Screening Goes Viral." Neuron 106, no. 1 (April 2020): 4–6. http://dx.doi.org/10.1016/j.neuron.2020.03.020.

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Guseh, Stephanie, Louise Wilkins-Haug, Anjali J. Kaimal, Lisa Dunn Albanese, and Kathryn J. Gray. "81: Utility of non-invasive genome-wide screening." American Journal of Obstetrics and Gynecology 222, no. 1 (January 2020): S67—S68. http://dx.doi.org/10.1016/j.ajog.2019.11.097.

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García, Patricia, Javier Encinar del Dedo, José Ayté, and Elena Hidalgo. "Genome-wide Screening of Regulators of Catalase Expression." Journal of Biological Chemistry 291, no. 2 (November 13, 2015): 790–99. http://dx.doi.org/10.1074/jbc.m115.696658.

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Dissertations / Theses on the topic "Genome wide screening"

Appari, Mahesh [Verfasser]. "Genome-wide screening of biomarkers in androgen insensitivity syndrome (AIS) / Mahesh Appari." Kiel : Universitätsbibliothek Kiel, 2009. http://d-nb.info/1019866764/34.

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Christ, Ryan. "Ancestral trees as weighted networks : scalable screening for genome wide association studies." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:8f382d56-2d5d-4a4f-9b39-41700897e02e.

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Several haplotype-based methods have been developed to identify loci where multiple mutations of low to moderate frequency and effect size modulate disease susceptibility. Most such approaches either do not scale to hundreds of thousands of genomes or do not explicitly model recombination and the block-like structure of haplotypes. Using a novel checkpointing technique and a C-core, vectorized implementation of an Hidden Markov Model (HMM) based on the Li & Stephens Model, at each single nucleotide polymorphism (SNP) along the genome, we obtain a local genetic distance between all pairs of haplotypes in a phased dataset. To rapidly test this local distance matrix for association with a phenotype, we derive two finite sample central limit type theorems for quadratic forms which do not require any further assumptions on the matrix other than it is free of outliers, for which we have an easily calculable, formal condition. We combine these results with a novel concentration inequality for Gaussian quadratic forms to upper and lower bound p-values for quadratic forms while avoiding a full eigendecomposition of each matrix. Applying our HMM implementation and quadratic form screening method, we recover known loci associated with malaria susceptibility and uncover new potential associations in a pilot dataset of 6,136 haplotypes.

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Löllgen, Ruth Mari Caroline. "Genome wide screening of loss of heterozygosity in human midgut carcinoid tumors with fluorescent technique." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972556702.

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Kaemena, Daniel Fraser. "CRISPR/Cas9 genome-wide loss of function screening identifies novel regulators of reprogramming to pluripotency." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31184.

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In 2006, Kazutoshi Takahashi and Shinya Yamanaka demonstrated the ability of four transcription factors; Oct4, Sox2, Klf4 and c-Myc to 'reprogram' differentiated somatic cells to a pluripotent state. This technology holds huge potential in the field of regenerative medicine, but reprogramming also a model system by which to the common regulators of all forced cell identity changes, for example, transdifferentiation. Despite this, the mechanism underlying reprogramming remains poorly understood and the efficiency of induced pluripotent stem cell (iPSC) generation, inefficient. One powerful method for elucidating the gene components influencing a biological process, such as reprogramming, is screening for a phenotype of interest using genome-wide mutant libraries. Historically, large-scale knockout screens have been challenging to perform in diploid mammalian genomes, while other screening technologies such as RNAi can be disadvantaged by variable knockdown of target transcripts and off-target effects. Components of clustered regularly interspaced short palindromic repeats and associated Cas proteins (CRISPR-Cas) prokaryote adaptive immunity systems have recently been adapted to edit genomic sequences at high efficiency in mammalian systems. Furthermore, the application of CRISPR-Cas components to perform proofof- principle genome-wide KO screens has been successfully demonstrated. I have utilised the CRISPR-Cas9 system to perform genome-wide loss-of-function screening in the context of murine iPSC reprogramming, identifying 18 novel inhibitors of reprogramming, in addition to four known inhibitors, Trp53, Cdkn1a, Jun, Dot1l and Gtf2i. Understanding how these novel reprogramming roadblocks function to inhibit the reprogramming process will provide insight into the molecular mechanisms underpinning forced cell identity changes.

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Löllgen, Ruth Mari Caroline. "Genome-wide screening of loss of heterozygosity in human midgut carcinoid tumors with fluorescent technique." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2004. http://dx.doi.org/10.18452/15047.

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Hintergrund: Karzinoid-Tumoren des embryonalen Mitteldarms sind seltene intestinale neuroendokrine Tumoren, bei denen zum Zeitpunkt der Diagnose häufig Metastasen vorliegen. Im Gegensatz zu Karzinoiden des Vorderdarms und Respirationstraktes sind sie nicht mit der Multiplen Endokrinen Neoplasie Typ 1 (MEN1) vergesellschaftet. Die Mechanismen ihrer Tumorigenesis sind weitgehend unbekannt. Methoden: Tumorgewebe acht sporadischer, maligner Dünndarm-Karzinoide war Objekt dieser Studie über Verlust der Heterozygotie ("Loss Of Heterozygosity" (LOH)) mit 131 fluoreszierenden Mikrosatelliten. DNA Sequenz-Analyse mit Oligonucleotid Primern, die Exon 8-11 des SMAD4/DPC4 Gens flankieren sowie immunhistochemische Färbung mit Smad4/DPC4 antikörpern wurde durchgeführt. Ergebnis: Chromosom 18 wies Deletionen in 88% der Tumoren auf. Alle außer einem Tumor hatten sowohl 18p als auch 18q verloren, in einem der Tumoren war eine kleine Region telomer zu den SMAD4/DPC4/DCC Genen auf 18q21 verloren. Andere Chromosomen waren nur in drei Tumoren betroffen. LOH auf Chromosom 11q13, dem MEN1 Lokus, wurde nicht gefunden.Sequenzierung der DNA und immunhistochemische Färbung für das SMAD4/DPC4 Gen zeigten keine Aberrationen. Diskussion: Die Funde der Chromosom 18 Deletionen weisen eindeutig auf ein entscheidendes Ereignis in der Tumorigenese von Karzinoiden des Mitteldarms hin. An der Entstehung dieser Tumoren könnte ein mutmaßliches Tumor Suppressor Gen beteiligt sein, welches auf Chromosom 18 lokalisiert ist. Dahingegen ist SMAD4/DPC4 wahrscheinlich nicht in die Tumorneogenese von Carcinois Tumoren involviert.
Background: Midgut carcinoid tumors are rare malignant tumors with origin in the neuroendocrine cells of the small intestine. Due to secretion of a variety of peptide hormones and biogenic amines they cause the carcinoid syndrome. Metastases are often present at first diagnosis. Despite this, patients have a realistic chance to survive for a prolonged period (30% (unresectable/metastatic disease) -79% (non-metastatic disease) 5-year survival rate) if treated by a combination of surgery and medication. Unlike their foregut counterparts, midgut carcinoid tumors are not or rarely associated with the multiple endocrine neoplasia type 1 (MEN1) syndrome. The genetic back-ground to tumorigenesis of these neoplasms is unknown. In contrast, the events involved in tumorigenesis of gastroenteropancreatic adenocarcinomas are better characterized with frequent mutations e.g. of the Smad4/DPC4, Smad2/MADR2/JV18-1 and DCC genes on chromosome 18. Methods: Eight metastatic midgut carcinoids were analysed by a genome-wide screening for loss of heterozygosity using 131 PCR-amplified fluorescent-labelled microsatellite markers. DNA sequence analysis using oligonucleotide primers flanking exons 8-11 of the Smad4/DPC4 gene and immunohistochemical staining with Smad4/DPC4 antibodies was performed. Results: Chromosome 18 was deleted in seven out of eight tumors (88%). All but one of these tumors had lost both 18p and 18q, the remaining tumor had lost the long arm but retained the short arm. Several other chromosomal alleles were lost in a subset of the tumors. Loss of heterozygosity (LOH) on chromosome 11q13, the MEN 1 locus, was not found. Smad4/DPC4 wild-type sequence and normal immunohistochemical staining for Smad4/DPC4 protein was found for all analysed tumors. Conclusions: Our finding of a high frequency of chromosome 18 deletions in 88% of the tumors strongly suggests that midgut carcinoid tumorigenesis might involve inactivation of a candidate tumor suppressor gene located in that region while Smad4/DPC4 is unlikely to be involved in that process. A more detailed analysis of the genetic events in midgut carcinoid tumors is warranted to clarify their neogenetic origin.

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Riehmer, Vera [Verfasser]. "Genome-wide screening methods in tumors of the central nervous system and cancer predisposition / Vera Riehmer." Bonn : Universitäts- und Landesbibliothek Bonn, 2014. http://d-nb.info/1054691770/34.

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Rudge, Felicity. "Genome-wide cDNA and RNAi screening to identify modulators of responses to a novel Wnt signalling inhibitor." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58589/.

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Wnt/β-catenin signalling plays a central role in the regulation of multicelluar organism development and in the maintenance of tissue homeostasis in adults. Dysregulation of Wnt signalling resulting in aberrant pathway activation is a key initiating step in the development of a diverse range of cancers, including colorectal cancer, and as such is an important target for therapeutic intervention. A novel Wnt pathway inhibitor, ‘MSC’, has been identified as blocking activated Wnt signalling, specifically through inhibiting the ability of CDK8 and CDK19 to activate nuclear β-catenin/TCF-dependent transcription. However, despite potently inhibiting Wnt-dependent transcription, the ability of MSC to reduce cellular viability was limited. This study aimed to determine genes that whose loss operated with MSC to reduce cell survival. A whole-genome RNAi chemical sensitisation screen identified 3 genes whose depletion in combination with MSC treatment conditionally reduced the viability of HCT116 cells in vitro. The outstanding hit of this screen was Histidyl Aminoacyl tRNA Synthetase (HARS). The identification of this enzyme as an MSC ‘interactor’ suggested links between Wnt signalling and the regulation of translation. BRAF and MED11 RNAi also conferred conditional sensitivity to MSC. Interestingly, MED11 is a component of the Mediator complex, a multiprotein transcription regulatory complex in which CDK8 functions to regulate β-catenin/TCF-dependent transcription, suggesting that mediator complex may be a key target of MSC action. A parallel overexpression screen was initiated to identify novel Wnt pathway activators, and subsequently used to map MSC resistance. Expression of the transcription factors GBX1 and HMGB2, determined to be novel regulators of TCF-dependent transcription, blocked MSC-mediated disruption of Wnt signalling. Overexpression of either gene in a clinical context might therefore be regarded as a contra-indication for MSC-class therapies. These studies have highlighted potential avenues for broadening the scope of MSC activity through the determination of survival and resistance mechanisms, thus the rational design of MSC-combination therapies could be of huge clinical benefit for the treatment of colorectal cancer.

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Stravalaci, Matteo. "Identification and characterization of mediators of toxicity of Aβ oligomers by genome wide screening in Caenorhabditis elegans." Thesis, Open University, 2017. http://oro.open.ac.uk/50285/.

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Soluble oligomers of the amyloid-β (Aβ) protein play a key role in the pathogenesis of Alzheimer’s disease (AD), although the underlying molecular mechanisms are poorly understood. In order to search for proteins involved in the formation and/or toxicity of Aβ oligomers, a transgenic C. elegans model of AD was used in which inducible expression of Aβ oligomers results in a complete paralysis; in these worms a genetic screen following chemical mutagenesis was applied to discover the genes involved in the Aβ-dependent paralysis (forward genetics). This analysis allowed identification of a mutated clone showing a complete lack of paralysis, despite this it not bear mutations in the Aβ coding region, and accumulates Aβ transcript and protein levels comparable to that of the non-mutated strain. This is the first in vivo model in which the expression of Aβ oligomers do not result in any toxic effect. The genome of the mutated worm was then sequenced and compared with that of the control strain to search for altered genes. Two genes, with no known function, were found to bear a stop codon mutation, likely resulting in the translation of an inactive protein. The rest of the mutations were missense mutations. Among them, point mutations were observed in some genes previously correlated with nematode lifespan and ageing. In C. elegans these biological processes are coordinated by the insulin/IGF-1-like signalling (IIS) pathway, which also regulates the response of the organism to toxic aggregated proteins. Thus, the activation of the IIS pathway was investigated in control and mutated worms. As expected, Aβ expression induced the up-regulation of two genes coding for small heat shock proteins (a class of chaperons known to be involved in AD) in the control strain, whereas these genes were actually down-regulated in the mutated strain. Since heat shock proteins are known to bind Aβ oligomers, these chaperons could directly mediate the formation of toxic amyloid species. Moreover, the results of the whole genome sequencing indicate that several proteins could act as potential novel mediators of Aβ toxicity and could open up new insights for research on age-related, neurodegenerative diseases.

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Sooda, Anuradha. "Discovery of novel HLA-B*57:01 restricted T-cell antigens through genome-wide screening of Epstein-Barr virus." Thesis, Sooda, Anuradha (2020) Discovery of novel HLA-B*57:01 restricted T-cell antigens through genome-wide screening of Epstein-Barr virus. PhD thesis, Murdoch University, 2020. https://researchrepository.murdoch.edu.au/id/eprint/54110/.

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A relationship between latent viral infections and drug hypersensitivity reactions (HSR) has been observed in several clinical situations. Abacavir hypersensitivity has been shown by several groups to be an HLA-B*57:01 restricted CD8+ T cell dependent process. Although compelling evidence suggests that carriage of HLA-B*57:01 is necessary, it is not sufficient for abacavir hypersensitivity. Based on previous structural and functional studies, it was hypothesised that heterologous immune responses of the pre-existing anti-viral T cell responses mediate abacavir hypersensitivity. Human herpesviruses (HHV) have been posited to be associated with the development of HSR because they have co-evolved with the human major histocompatibility complex and they persist in most people as lifelong latent, asymptomatic infections. In addition, they are reactivated in immunocompromised individuals and have been implicated in drug-viral interactions such as associated with Epstein-Barr virus (EBV). EBV is the most common HHV infecting more than 95% of the world’s population. The EBV genome is approximately 172 kb in length and encodes 89 proteins. However, the extent to which these proteins are surveyed by host-derived T cells has not been fully explored. The objective of this body of work was to generate ORFeome-wide map of memory CD8+ T cell responses for the identification of HLA-B*57:01 restricted antigens which could be involved in the cross-reactivity of abacavir drug hypersensitivity. Mapping revealed 14 novel HLA-B*57:01 restricted EBV antigens and confirmed the previously identified epitopes EBNA3B (VSFIEFVGW), EBNA2 (LASAMRML), and LMP1 (IALYLQQNW). A novel immunodominant epitope was detected in EBNA3C (QSRGDENRGW). To identify cross-reactive anti-viral T cell receptors, single cells specific for the immunodominant epitopes of EBNA3B (VSF) and EBNA3C (QSR) were sorted based on tetramer staining. Antigen-specific T cells were sequenced for the T cell receptors cloned into Jurkat cells. A modified heterologous T cell receptor reporter assay was developed to study the T cell responses against HLA-B*57:01 restricted EBV immunodominant epitopes. Dose-dependent T cell responses were detected against each EBV epitope, however, the TCRs were not cross-reactive to abacavir plus self-peptide presented in the context of HLA-B*57:01. The presence of abacavir was shown to modulate the EBV-specific TCR responses to the two EBV epitopes, which suggested the non-covalent binding of abacavir to HLA-B*57:01 may have down modulated the TCR responses. Although unable to demonstrate cross-reactivity of the EBV-specific TCRs with the abacavir plus self-peptide, this work has provided a road map for future experiments to elucidate the role of heterologous immunity in the immunopathogenesis of drug hypersensitivity and other aberrant acquired immune responses in humans.

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Lawson, Jonathan Luke Done. "Genome-wide microscopy screening identifies links across processes including a conserved connection between DNA damage control and the microtubule cytoskeleton." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/253007.

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Previous PhD students in the lab created a method for large-scale, high-content microscopy screening of a cell library consisting of over 3000 single mutant strains of the fission yeast, Schizosaccharomyces pombe. Each strain has one nonessential gene knocked-out, allowing investigation of the resulting phenotypes. I report the implementation and completion of this screen; developing methods to ensure reliable and accurate results through inclusion of many controls across multiple screening repeats. In total, over 4.5 million images from approximately 19 000 biologically independent cell populations were imaged and analysed. All strains screened contained GFP-labelled tubulin (GFP-Atb2) allowing visualisation of the microtubule polymer network and its organisation in cells, a feature that is conserved across eukaryotes and simplified in S. pombe, making it easy to study. Examination of cell outlines and microtubule patterns was used to study three cell processes: the shape of cells, the organisational pattern of interphase microtubules and the cell cycle stage of cells, as judged by microtubule pattern. Comparison with extensive data from wild-type cells led to the identification of 262 factors that influence one or more of these cell processes. I go on to biologically validate some of the outcomes from the screen, leading to a publication in Developmental Cell reporting the screen, its findings and the online genomic resource SYSGRO. I then focus on a group of mutants that suggest a connection between the DNA damage response (DDR) and microtubule organisation. From here I show that the DDR induces elongation of microtubule bundles in response to the DDR kinases, ATM and ATR. I begin to reveal factors that may mediate this response and finally, I provide evidence to suggest that the same mechanism is conserved in cultured human cells (Hc3716-hTERT), which may go some way to explaining clinical results showing a beneficial effect of microtubule destabilisation in conjunction with cancer therapies.

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Books on the topic "Genome wide screening"

Casanova, Nancy G., Ting Wang, Eddie T. Chiang, and Joe G. N. Garcia. Genomics, Epigenetics, and Precision Medicine in Integrative Preventive Medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190241254.003.0004.

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This chapter briefly reviews the use of genomewide screening for early detection, treatment, and prevention and the utility of genome-based biomarkers as a tool for precision medicine and its application to population and integrative preventive medicine. Advances in technology have made genomic screening more affordable and widely available, and both our understanding and the value of testing grow as more data is collected. Even more recently, the growing availability of epigenetic testing, methylation and ROS-associated molecular signatures are providing more insight into dynamic aspects of the human genome and how lifestyle and IPM change affect the expression of the genome. Early adoption of precision medicine in oncology offers a model that should be expanded into wider areas of treatment and prevention.

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Tülümen, Erol, and Martin Borggrefe. Monogenic and oligogenic cardiovascular diseases: genetics of arrhythmias—short QT syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0150.

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Short QT syndrome (SQTS) is a very rare, sporadic or autosomal dominant inherited channelopathy characterized by abnormally short QT intervals on the electrocardiogram and increased propensity to atrial and ventricular tachyarrhythmias and/or sudden cardiac death. Since its recognition as a distinct clinical entity in 2000, significant progress has been made in defining the clinical, molecular, and genetic basis of SQTS. To date, several causative gain-of-function mutations in potassium channel genes and loss-of-function mutations in calcium channel genes have been identified. The physiological consequence of these mutations is an accelerated repolarization, thus abbreviated action potentials and shortened QT interval with an increased inhomogeneity and dispersion of repolarization. Regarding other rare monogenetic arrhythmias, a genetic basis of atrial fibrillation was considered very unlikely until very recently. However, in the last decade the heritability of atrial fibrillation in the general population has been well described in several epidemiological studies. So far, more than 30 genes have been implicated in atrial fibrillation through candidate gene approach studies, and 14 loci were found to be associated with atrial fibrillation through genome-wide association studies. This genetic heterogeneity and the low prevalence of mutations in any single gene restrict the clinical utility of genetic screening in atrial fibrillation.

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Book chapters on the topic "Genome wide screening"

Wertz, Mary H., and Myriam Heiman. "Genome-Wide Genetic Screening in the Mammalian CNS." In Research and Perspectives in Neurosciences, 31–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60192-2_3.

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Zhou, Xiaobo, K. Y. Liu, P. Bradley, N. Perrimon, and Stephen TC Wong. "Towards Automated Cellular Image Segmentation for RNAi Genome-Wide Screening." In Lecture Notes in Computer Science, 885–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11566465_109.

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Guijarro, Maria V., and Amancio Carnero. "Genome-Wide miRNA Screening for Genes Bypassing Oncogene-Induced Senescence." In Methods in Molecular Biology, 53–68. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6670-7_5.

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O’Reilly, Linda P., Ryan R. Knoerdel, Gary A. Silverman, and Stephen C. Pak. "High-Throughput, Liquid-Based Genome-Wide RNAi Screening in C. elegans." In Methods in Molecular Biology, 151–62. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6337-9_12.

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Horton, Brooke N., and Anuj Kumar. "Genome-Wide Synthetic Genetic Screening by Transposon Mutagenesis in Candida albicans." In Gene Essentiality, 125–35. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2398-4_8.

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Chen, Xiaochu, and Lan Xu. "Genome-Wide RNAi Screening to Dissect the TGF-β Signal Transduction Pathway." In Methods in Molecular Biology, 365–77. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2966-5_24.

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Cao, Xiuling, Xuejiao Jin, and Beidong Liu. "Genome-Wide Imaging-Based Phenomic Screening Using Yeast (Saccharomyces cerevisiae) Strain Collections." In Methods in Molecular Biology, 85–95. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0868-5_8.

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Wajapeyee, Narendra, Sara K. Deibler, and Michael R. Green. "Genome-Wide RNAi Screening to Identify Regulators of Oncogene-Induced Cellular Senescence." In Methods in Molecular Biology, 373–82. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-239-1_25.

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Scarborough, Anna M., Ashwin Govindan, and Nicholas K. Conrad. "Genome-Wide CRISPR Screening to Identify Mammalian Factors that Regulate Intron Retention." In Methods in Molecular Biology, 263–84. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2521-7_16.

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Adelmann, Charles H., Tim Wang, David M. Sabatini, and Eric S. Lander. "Genome-Wide CRISPR/Cas9 Screening for Identification of Cancer Genes in Cell Lines." In Methods in Molecular Biology, 125–36. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8967-6_10.

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Conference papers on the topic "Genome wide screening"

Elster, Dana, Marie Tollot, Karin Schlegelmilch, Alessandro Ori, Andreas Rosenwald, Erik Sahai, and Björn von Eyss. "Abstract PR05: Genome-wide screening identifies novel YAP modulators." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-pr05.

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Tedesco, Donato, Paul Diehl, Mikhail Makhanov, Sylvain Baron, Dmitry Suchkov, and Alex Chenchik. "Abstract C161: CRISPR/Cas9 genome-wide gRNA library screening platform." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c161.

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Abdelmanova, Alexandra S., Alexander A. Sermyagin, Arsen V. Dotsev, Nikolay V. Bardukov, Margaret S. Fornara, Gottfried Brem, and Natalia A. Zinovieva. "Genome-Wide Screening for SNPs Associated with Stature in Diverse Cattle Breeds." In The 2nd International Electronic Conference on Diversity (IECD 2022)—New Insights into the Biodiversity of Plants, Animals and Microbes. Basel Switzerland: MDPI, 2022. http://dx.doi.org/10.3390/iecd2022-12415.

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Beckett, AR, S. McKinney, SS Poon, J. Fee, and SA Aparicio. "Identifying stromal-epithelial interactions in the mammary gland through genome-wide siRNA screening." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-101.

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Cramer, Paul, and Björn von Eyss. "Abstract B24: Identification of YAP modulators using genome-wide gain-of-function screening." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-b24.

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Wang, Jun, Xiaobo Zhou, Fuhai Li, and Stephen Wong. "Classify cellular phenotype in high-throughput fluorescence microcopy images for RNAi genome-wide screening." In 2006 IEEE/NLM Life Science Systems and Applications Workshop. IEEE, 2006. http://dx.doi.org/10.1109/lssa.2006.250404.

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de Vos, Bob D., Jessica van Setten, Pim A. de Jong, Willem P. Mali, Matthijs Oudkerk, Max A. Viergever, and Ivana Išgum. "Genome-wide association study of coronary and aortic calcification in lung cancer screening CT." In SPIE Medical Imaging, edited by Martin A. Styner and Elsa D. Angelini. SPIE, 2016. http://dx.doi.org/10.1117/12.2217024.

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Kang, Zhigang, and Liang Cao. "Abstract 254: Genome-wide shRNA screening identifies candidate proteins modulating the extrinsic apoptotic pathway." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-254.

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Lu, Tzu-Pin, Pei-Chun Chen, Jang-Ming Lee, Chung-Ping Hsu, Shin-Kuang Chen, Mong-Hsun Tsai, Chuhsing K. Hsiao, Eric Y. Chuang, and Liang-Chuan Lai. "Abstract 2944: Genome-wide transcriptional modulation screening in non-smoking female lung cancer in Taiwan." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2944.

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Beckett, M., Y. Shi, H. Blair, A. Krippner-Heidenreich, and F. van Delft. "In vitro and in vivo genome wide CRISPR screening under drug treatment in T-ALL." In 31. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1644989.

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Reports on the topic "Genome wide screening"

Lehman, Donna, Robin Leach, and August Blackburn. Assessing the Role of Copy Number Variants in Prostate Cancer Risk and Progression Using a Novel Genome-Wide Screening Method. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada542445.

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Lehman, Donna, August Blackburn, and Robin Leach. Assessing the Role of Copy Number Variants in Prostate Cancer Risk and Progression using a Novel Genome-Wide Screening Method. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568305.

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Lehman, Donna, and Robin Leach. Assessing the Role of Copy Number Variants in Prostate Cancer Risk and Progression Using a Novel Genome-Wide Screening Method. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada594060.

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Lehman, Donna. Assessing the Role of Copy Number Variants in Prostate Cancer Risk and Progression Using a Novel Genome-Wide Screening Method. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada554128.

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Shpigel, Nahum Y., Ynte Schukken, and Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699853.bard.

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Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. E. coli are a leading cause of acute mastitis in dairy animals worldwide and certainly in Israel and North America. The species E. coli comprises a highly heterogeneous group of pathogens, some of which are commensal residents of the gut, infecting the mammary gland after contamination of the teat skin from the environment. As compared to other gut microflora, mammary pathogenic E. coli (MPEC) may have undergone evolutionary adaptations that improve their fitness for colonization of the unique and varied environmental niches found within the mammary gland. These niches include competing microbes already present or accompanying the new colonizer, soluble and cellular antimicrobials in milk, and the innate immune response elicited by mammary cells and recruited immune cells. However, to date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. The original overall research objective of this application was to develop a genome-wide, transposon-tagged mutant collection of MPEC strain P4 and to use this technology to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. In the course of the project we decided to take an alternative genome-wide approach and to use whole genomes bioinformatics analysis. Using genome sequencing and analysis of six MPEC strains, our studies have shown that type VI secretion system (T6SS) gene clusters were present in all these strains. Furthermore, using unbiased screening of MPEC strains for reduced colonization, fitness and virulence in the murine mastitis model, we have identified in MPEC P4-NR a new pathogenicity island (PAI-1) encoding the core components of T6SS and its hallmark effectors Hcp, VgrG and Rhs. Next, we have shown that specific deletions of T6SS genes reduced colonization, fitness and virulence in lactating mouse mammary glands. Our long-term goal is to understand the molecular mechanisms of host-pathogen interactions in the mammary gland and to relate these mechanisms to disease processes and pathogenesis. We have been able to achieve our research objectives to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. The project elucidated a new basic concept in host pathogen interaction of MPEC, which for the best of our knowledge was never described or investigated before. This research will help us to shed new light on principles behind the infection strategy of MPEC. The new targets now enable prevalence and epidemiology studies of T6SS in field strains of MPEC which might unveil new geographic, management and ecological risk factors. These will contribute to development of new approaches to treat and prevent mastitis by MPEC and perhaps other mammary pathogens. The use of antibiotics in farm animals and specifically to treat mastitis is gradually precluded and thus new treatment and prevention strategies are needed. Effective mastitis vaccines are currently not available, structural components and effectors of T6SS might be new targets for the development of novel vaccines and therapeutics.

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Bercovier, Herve, and Ronald P. Hedrick. Diagnostic, eco-epidemiology and control of KHV, a new viral pathogen of koi and common carp. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7695593.bard.

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Original objectives and revisions-The proposed research included these original objectives: field validation of diagnostic tests (PCR), the development and evaluation of new sensitive tools (LC-PCR/TaqManPCR, antibody detection by ELISA) including their use to study the ecology and the epidemiology of KHV (virus distribution in the environment and native cyprinids) and the carrier status of fish exposed experimentally or naturally to KHV (sites of virus replication and potential persistence or latency). In the course of the study we completed the genome sequence of KHV and developed a DNA array to study the expression of KHV genes in different conditions. Background to the topics-Mass mortality of koi or common carp has been observed in Israel, USA, Europe and Asia. These outbreaks have reduced exports of koi from Israel and have created fear about production, import, and movements of koi and have raised concerns about potential impacts on native cyprinid populations in the U.S.A. Major conclusions-A suite of new diagnostic tools was developed that included 3 PCR assays for detection of KHV DNA in cell culture and fish tissues and an ELISA assay capable of detecting anti-KHV antibodies in the serum of koi and common carp. The TKPCR assay developed during the grant has become an internationally accepted gold standard for detection of viral DNA. Additionally, the ELISA developed for detecting serum anti-KHV antibodies is now in wide use as a major nonlethal screening tool for evaluating virus status of koi and common carp populations. Real time PCR assays have been able to detect viral DNA in the internal organs of survivors of natural and wild type vaccine exposures at 1 and 10³ genome equivalents at 7 months after exposure. In addition, vaccinated fish were able to transmit the virus to naive fish. Potential control utilizing hybrids of goldfish and common carp for production demonstrated they were considerably more resistant than pure common carp or koi to both KHV (CyHV-3). There was no evidence that goldfish or other tested endemic cyprinids species were susceptible to KHV. The complete genomic sequencing of 3 strains from Japan, the USA, and Israel revealed a 295 kbp genome containing a 22 kbp terminal direct repeat encoding clear gene homologs to other fish herpesviruses in the family Herpesviridae. The genome encodes156 unique protein-coding genes, eight of which are duplicated in the terminal repeat. Four to seven genes are fragmented and the loss of these genes may be associated with the high virulence of the virus. Viral gene expression was studies by a newly developed chip which has allowed verification of transcription of most all hypothetical genes (ORFs) as well as their kinetics. Implications, both scientific and agricultural- The results from this study have immediate application for the control and management of KHV. The proposal provides elements key to disease management with improved diagnostic tools. Studies on the ecology of the virus also provide insights into management of the virus at the farms that farmers will be able to apply immediately to reduce risks of infections. Lastly, critical issues that surround present procedures used to create “resistant fish” must be be resolved (e.g. carriers, risks, etc.). Currently stamping out may be effective in eradicating the disease. The emerging disease caused by KHV continues to spread. With the economic importance of koi and carp and the vast international movements of koi for the hobby, this disease has the potential for even further spread. The results from our studies form a critical component of a comprehensive program to curtail this emerging pathogen at the local, regional and international levels.

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Li, Li, Joseph Burger, Nurit Katzir, Yaakov Tadmor, Ari Schaffer, and Zhangjun Fei. Characterization of the Or regulatory network in melon for carotenoid biofortification in food crops. United States Department of Agriculture, April 2015. http://dx.doi.org/10.32747/2015.7594408.bard.

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The general goals of the BARD research grant US-4423-11 are to understand how Or regulates carotenoid accumulation and to reveal novel strategies for breeding agricultural crops with enhanced β-carotene level. The original objectives are: 1) to identify the genes and proteins in the Or regulatory network in melon; 2) to genetically and molecularly characterize the candidate genes; and 3) to define genetic and functional allelic variation of these genes in a representative germplasm collection of the C. melo species. Or was found by the US group to causes provitamin A accumulation in chromoplasts in cauliflower. Preliminary genetic study from the Israeli group revealed that the melon Or gene (CmOr) completely co-segregated with fruit flesh color in a segregating mapping population and in a wide melon germplasm collection, which set the stage for the funded research. Major conclusions and achievements include: 1). CmOris proved to be the gene that controls melon fruit flesh color and represents the previously described gflocus in melon. 2). Genetic and molecular analyses of CmOridentify and confirm a single SNP that is responsible for the orange and non-orange phenotypes in melon fruit. 3). Alteration of the evolutionarily conserved arginine in an OR protein to both histidine or alanine greatly enhances its ability to promote carotenoid accumulation. 4). OR promotes massive carotenoid accumulation due to its dual functions in regulating both chromoplast biogenesis and carotenoid biosynthesis. 5). A bulk segregant transcriptome (BSRseq) analysis identifies a list of genes associated with the CmOrregulatory network. 6). BSRseq is proved to be an effective approach for gene discovery. 7). Screening of an EMS mutation library identifies a low β mutant, which contains low level of carotenoids due to a mutation in CmOrto produce a truncated form of OR protein. 8). low β exhibits lower germination rate and slow growth under salt stress condition. 9). Postharvest storage of fruit enhances carotenoid accumulation, which is associated with chromoplast development. Our research uncovers the molecular mechanisms underlying the Or-regulated high level of carotenoid accumulation via regulating carotenoidbiosynthetic capacity and storage sink strength. The findings provide mechanistic insights into how carotenoid accumulation is controlled in plants. Our research also provides general and reliable molecular markers for melon-breeding programs to select orange varieties, and offers effective genetic tools for pro-vitamin A enrichment in other important crops via the rapidly developed genome editing technology. The newly discovered low β mutant could lead to a better understanding of the Or gene function and its association with stress response, which may explain the high conservation of the Or gene among various plant species.

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Cohen, Roni, Kevin Crosby, Menahem Edelstein, John Jifon, Beny Aloni, Nurit Katzir, Haim Nerson, and Daniel Leskovar. Grafting as a strategy for disease and stress management in muskmelon production. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7613874.bard.

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The overall objective of this research was to elucidate the horticultural, pathological, physiological and molecular factors impacting melon varieties (scion) grafted onto M. cannonballus resistant melon and squash rootstocks. Specific objectives were- to compare the performance of resistant melon germplasm (grafted and non-grafted) when exposed to M. cannoballus in the Lower Rio Grande valley and the Wintergarden, Texas, and in the Arava valley, Israel; to address inter-species relationships between a Monosporascus resistant melon rootstock and susceptible melon scions in terms of fruit-set, fruit quality and yield; to study the factors which determine the compatibility between the rootstock and the scion in melon; to compare the responses of graft unions of differing compatibilities under disease stress, high temperatures, deficit irrigation, and salinity stress; and to investigate the effect of rootstock on stress related gene expression in the scion. Some revisions were- to include watermelon in the Texas investigations since it is much more economically important to the state, and also to evaluate additional vine decline pathogens Didymella bryoniae and Macrophomina phaseolina. Current strategies for managing vine decline rely heavily on soil fumigation with methyl bromide, but restrictions on its use have increased the need for alternative management strategies. Grafting of commercial melon varieties onto resistant rootstocks with vigorous root systems is an alternative to methyl bromide for Monosporascus root rot/vine decline (MRR/VD) management in melon production. Extensive selection and breeding has already produced potential melon rootstock lines with vigorous root systems and disease resistance. Melons can also be grafted onto Cucurbita spp., providing nonspecific but efficient protection from a wide range of soil-borne diseases and against some abiotic stresses, but compatibility between the scion and the rootstock can be problematic. During the first year experiments to evaluate resistance to the vine decline pathogens Monosporascus cannonballus, Didymella bryoniae, and Macrophomina phaseolina in melon and squash rootstocks proved the efficacy of these grafted plants in improving yield and quality. Sugars and fruit size were better in grafted versus non-grafted plants in both Texas and Israel. Two melons (1207 and 124104) and one pumpkin, Tetsukabuto, were identified as the best candidate rootstocks in Texas field trials, while in Israel, the pumpkin rootstock RS59 performed best. Additionally, three hybrid melon rootstocks demonstrated excellent resistance to both M. cannonballus and D. bryoniae in inoculated tests, suggesting that further screening for fruit quality and yield should be conducted. Experiments with ABA in Uvalde demonstrated a significant increase in drought stress tolerance and concurrent reduction in transplant shock due to reduced transpiration for ‘Caravelle’ plants. In Israel, auxin was implicated in reducing root development and contributing to increased hydrogen peroxide, which may explain incompatibility reactions with some squash rootstocks. However, trellised plants responded favorably to auxin (NAA) application at the time of fruit development. Gene expression analyses in Israel identified several cDNAs which may code for phloem related proteins, cyclins or other factors which impact the graft compatibility. Manipulation of these genes by transformation or traditional breeding may lead to improved rootstock cultivars. Commercial applications of the new melon rootstocks as well as the ABA and TIBA growth regulators have potential to improve the success of grafted melons in both Israel and Texas. The disease resistance, fruit quality and yield data generated by the field trials will help producers in both locations to decide what rootstock/scion combinations will be best.

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Dolja, Valerian V., Amit Gal-On, and Victor Gaba. Suppression of Potyvirus Infection by a Closterovirus Protein. United States Department of Agriculture, March 2002. http://dx.doi.org/10.32747/2002.7580682.bard.

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The plant virus family Polyviridae is the largest and most destructive of all plant viruses. Despite the continuous effort to develop resistant plant varieties, there is a desperate need for novel approaches conferring wide-range potyvirus resistance. Based on experiments with the tobacco etch potyvirus (TEV)-derived gene expression vector, we suggested approach for screening of the candidate resistance genes. This approach relies on insertion of the genes into a virus vector and evaluation of the phenotypes of the resulting recombinant viruses. The genes which suppress infection by the recombinant virus are selected as candidates for engineering transgenic resistance. Our analysis of the TEV variants expressing proteins of the beet yellows closterovirus (BYV) revealed that one of those, the leader proteinase (L-Pro), strongly and specifically interfered with the hybrid TEV infection. Since closterovirus L-Pro is evolutionary related to potyviral helper component-proteinase (HC-Pro), we suggested that the L-Pro interfered with HC-Pro function via a trans-dominant inhibitory effect. Based on these findings, we proposed to test two major hypotheses. First, we suggested that L-Pro-mediated suppression of potyvirus infection is a general phenomenon effective against a range of potyviruses. The second hypothesis stated that the suppression effect can be reproduced in transgenic plants expressing L-Pro, and can be utilized for generation of resistance to potyviruses. In accord with these hypotheses, we developed two original objectives of our proposal: A) to determine the range of the closterovirus-derived suppression of potyviral infection, and B) to try and utilize the L-Pro-mediated suppression for the development of transgenic resistance to potyviruses. In the first phase of the project, we have developed all major tools and technologies required for successful completion of the proposed research. These included TEV and ZYMV vectors engineered to express several closteroviral L-Pro variants, and generation of the large collection of transgenic plants. To our satisfaction, characterization of the infection phenotypes exhibited by chimeric TEV and ZYMV variants confirmed our first hypothesis. For instance, similar to TEV-L- Pro(BYV) chimera, ZYMV-L-Pro(LIYV) chimera was debilitated in its systemic spread. In contrast, ZYMV-GUS chimera (positive control) was competent in establishing vigorous systemic infection. These and other results with chimeric viruses indicated that several closteroviral proteinases inhibit long-distance movement of the potyviruses upon co-expression in infected plants. In order to complete the second objective, we have generated ~90 tobacco lines transformed with closteroviral L-Pro variants, as well as ~100 lines transformed with BYV Hsp70-homolog (Hsp70h; a negative control). The presence and expression of the trans gene in each line was initially confirmed using RT-PCR and RNA preparations isolated from plants. However, since detection of the trans gene-specific RNA can not guarantee production of the corresponding protein, we have also generated L-Pro- and Hsp70h-specific antisera using corresponding synthetic peptides. These antisera allowed us to confirm that the transgenic plant lines produced detectable, although highly variable levels of the closterovirus antigens. In a final phase of the project, we tested susceptibility of the transgenic lines to TEV infection. To this end, we determined that the minimal dilution of the TEV inoculum that is still capable of infecting 100% of nontransgenic plants was 1:20, and used 10 plants per line (in total, ~2,000 plants). Unfortunately, none of the lines exhibited statistically significant reduction in susceptibility. Although discouraging, this outcome prompted us to expand our experimental plan and conduct additional experiments. Our aim was to test if closteroviral proteinases are capable of functioning in trans. We have developed agroinfection protocol for BYV, and tested if co- expression of the L-Pro is capable of rescuing corresponding null-mutant. The clear-cut, negative results of these experiments demonstrated that L-Pro acts only in cis, thus explaining the lack of resistance in our transgenic plants. We have also characterized a collection of the L-Pro alanine- scanning mutants and found direct genetic evidence of the requirement for L-Pro in virus systemic spread. To conclude, our research supported by BARD confirmed one but not another of our original hypotheses. Moreover, it provided an important insight into functional specialization of the viral proteinases and generated set of tools and data with which we will be able to address the molecular mechanisms by which these proteins provide a variety of critical functions during virus life cycle.

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Manulis, Shulamit, Christine D. Smart, Isaac Barash, Guido Sessa, and Harvey C. Hoch. Molecular Interactions of Clavibacter michiganensis subsp. michiganensis with Tomato. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7697113.bard.

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Clavibacter michiganensis subsp. michiganensis (Cmm), the causal agent of bacterial wilt and canker of tomato, is the most destructive bacterial disease of tomato causing substantial economic losses in Israel, the U.S.A. and worldwide. The molecular strategies that allow Cmm, a Gram-positive bacterium, to develop a successful infection in tomato plants are largely unknown. The goal of the project was to elucidate the molecular interactions between Cmmand tomato. The first objective was to analyze gene expression profiles of susceptible tomato plants infected with pathogenic and endophytic Cmmstrains. Microarray analysis identified 122 genes that were differentially expressed during early stages of infection. Cmm activated typical basal defense responses in the host including induction of defense-related genes, production of scavenging of free oxygen radicals, enhanced protein turnover and hormone synthesis. Proteomic investigation of the Cmm-tomato interaction was performed with Multi-Dimensional Protein Identification Technology (MudPIT) and mass spectroscopy. A wide range of enzymes secreted by Cmm382, including cell-wall degrading enzymes and a large group of serine proteases from different families were identified in the xylem sap of infected tomato. Based on proteomic results, the expression pattern of selected bacterial virulence genes and plant defense genes were examined by qRT-PCR. Expression of the plasmid-borne cellulase (celA), serine protease (pat-1) and serine proteases residing on the chp/tomA pathogenicity island (chpCandppaA), were significantly induced within 96 hr after inoculation. Transcription of chromosomal genes involved in cell wall degradation (i.e., pelA1, celB, xysA and xysB) was also induced in early infection stages. The second objective was to identify by VIGS technology host genes affecting Cmm multiplication and appearance of disease symptoms in plant. VIGS screening showed that out of 160 tomato genes, which could be involved in defense-related signaling, suppression of 14 genes led to increase host susceptibility. Noteworthy are the genes Snakin-2 (inhibitor of Cmm growth) and extensin-like protein (ELP) involved in cell wall fortification. To further test the significance of Snakin -2 and ELP in resistance towards Cmm, transgenic tomato plants over-expressing the two genes were generated. These plants showed partial resistance to Cmm resulting in a significant delay of the wilt symptoms and reduction in size of canker lesion compared to control. Furthermore, colonization of the transgenic plants was significantly lower. The third objective was to assess the involvement of ethylene (ET), jasmonate (JA) and salicylic acid (SA) in Cmm infection. Microarray and proteomic studies showed the induction of enzymes involved in ET and JA biosynthesis. Cmm promoted ET production 8 days after inoculation and SIACO, a key enzyme of ET biosynthesis, was upregulated. Inoculation of the tomato mutants Never ripe (Nr) impaired in ET perception and transgenic plants with reduced ET synthesis significantly delayed wilt symptoms as compared to the wild-type plants. The retarded wilting in Nr plants was shown to be a specific effect of ET insensitivity and was not due to altered expression of defense related genes, reduced bacterial population or decrease in ethylene biosynthesis . In contrast, infection of various tomato mutants impaired in JA biosynthesis (e.g., def1, acx1) and JA insensitive mutant (jai1) yielded unequivocal results. The fourth objective was to determine the role of cell wall degrading enzymes produced by Cmm in xylem colonization and symptoms development. A significance increase (2 to 7 fold) in expression of cellulases (CelA, CelB), pectate lyases (PelA1, PelA2), polygalacturonase and xylanases (XylA, XylB) was detected by qRT-PCR and by proteomic analysis of the xylem sap. However, with the exception of CelA, whose inactivation led to reduced wilt symptoms, inactivation of any of the other cell wall degrading enzymes did not lead to reduced virulence. Results achieved emphasized the complexity involved in Cmm-tomato interactions. Nevertheless they provide the basis for additional research which will unravel the mechanism of Cmm pathogenicity and formulating disease control measures.

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