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10 results on '"Tanya Kutyavin"'

1. Highly Parallel Quantification and Compartment Localization of Transcription Factors and Nuclear Proteins

Author

Alexander J. Federation, Vivek Nandakumar, Brian C. Searle, Andrew Stergachis, Hao Wang, Lindsay K. Pino, Gennifer Merrihew, Ying S. Ting, Nicholas Howard, Tanya Kutyavin, Michael J. MacCoss, and John A. Stamatoyannopoulos

Subjects
Biology (General), QH301-705.5
Abstract

Summary: Transcription factors and other chromatin-associated proteins are difficult to quantify comprehensively. Here, we combine facile nuclear sub-fractionation with data-independent acquisition mass spectrometry to achieve rapid, sensitive, and highly parallel quantification of the nuclear proteome in human cells. We apply this approach to quantify the response to acute degradation of BET bromodomains, revealing unexpected chromatin regulatory dynamics. The method is simple and enables system-level study of previously inaccessible chromatin and genome regulators. : Proteins that bind DNA and regulate the expression of genes are difficult to measure accurately. In this study, we present a method that quantifies these proteins with high coverage and in high throughput, providing a system-wide view of protein dynamics on chromatin. Keywords: data-independent acquisition, transcription factors, proteomics, chromatin, small molecule degredation

Published
2020
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2. Widespread site-dependent buffering of human regulatory polymorphism.

Author

Matthew T Maurano, Hao Wang, Tanya Kutyavin, and John A Stamatoyannopoulos

Subjects
Genetics, QH426-470
Abstract

The average individual is expected to harbor thousands of variants within non-coding genomic regions involved in gene regulation. However, it is currently not possible to interpret reliably the functional consequences of genetic variation within any given transcription factor recognition sequence. To address this, we comprehensively analyzed heritable genome-wide binding patterns of a major sequence-specific regulator (CTCF) in relation to genetic variability in binding site sequences across a multi-generational pedigree. We localized and quantified CTCF occupancy by ChIP-seq in 12 related and unrelated individuals spanning three generations, followed by comprehensive targeted resequencing of the entire CTCF-binding landscape across all individuals. We identified hundreds of variants with reproducible quantitative effects on CTCF occupancy (both positive and negative). While these effects paralleled protein-DNA recognition energetics when averaged, they were extensively buffered by striking local context dependencies. In the significant majority of cases buffering was complete, resulting in silent variants spanning every position within the DNA recognition interface irrespective of level of binding energy or evolutionary constraint. The prevalence of complex partial or complete buffering effects severely constrained the ability to predict reliably the impact of variation within any given binding site instance. Surprisingly, 40% of variants that increased CTCF occupancy occurred at positions of human-chimp divergence, challenging the expectation that the vast majority of functional regulatory variants should be deleterious. Our results suggest that, even in the presence of "perfect" genetic information afforded by resequencing and parallel studies in multiple related individuals, genomic site-specific prediction of the consequences of individual variation in regulatory DNA will require systematic coupling with empirical functional genomic measurements.

Published
2012
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3. Quantification of nuclear protein dynamics reveals chromatin remodeling during acute protein degradation

Author

Brian C. Searle, Tanya Kutyavin, Ying S. Ting, Vivek Nandakumar, Michael J. MacCoss, Alexander J. Federation, Nicholas P. Howard, Lindsay K. Pino, John A. Stamatoyannopoulos, Gennifer E. Merrihew, and Hao Wang

Subjects
Nucleoplasm, Euchromatin, Chemistry, Proteome, Nuclear protein, Protein degradation, Chromatin remodeling, Bromodomain, Chromatin, Cell biology
Abstract

Sequencing-based technologies cannot measure post-transcriptional dynamics of the nuclear proteome, but unbiased mass-spectrometry measurements of chromatin-associated proteins remain difficult. In this work, we have combined facile nuclear sub-fractionation approaches with data-independent acquisition mass spectrometry to improve detection and quantification of nuclear proteins in human cells and tissues. Nuclei are isolated and subjected to a series of extraction conditions that enrich for nucleoplasm, euchromatin, heterochromatin and nuclear-membrane associated proteins. Using this approach, we can measure peptides from over 70% of the expressed nuclear proteome. As we are physically separating chromatin compartments prior to analysis, proteins can be assigned into functional chromatin environments to illuminate systems-wide nuclear protein dynamics. The integrity of nuclear sub-compartments were validated with immunofluorescence, which confirms the presence of key markers during chromatin extraction. We then apply this method to study the nuclear proteome-wide response to pharmacological degradation of the BET bromodomain proteins. BET degradation leads to widespread changes in chromatin composition, and we discover global HDAC1/2-mediated remodeling of chromatin previously bound by BET bromodomains. In summary, we have developed a technology for reproducible, comprehensive characterization of the nuclear proteome to observe the systems-wide nuclear protein dynamics.

Published
2018
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4. Systematic Localization of Common Disease-Associated Variation in Regulatory DNA

Author

Hongzhu Qu, Peter J. Sabo, Steven F. Ziegler, Ian A. Glass, Rajinder Kaul, Shelly Heimfeld, Shamil R. Sunyaev, Eric Rynes, Jennifer A. Brody, Tanya Kutyavin, R. Scott Hansen, Chris Cotsapas, Daniel Bates, Robert E. Thurman, Matthew T. Maurano, Shane Neph, Anthony Shafer, Sandra Stehling-Sun, Nona Sotoodehnia, Eric Haugen, Fidencio Neri, Theresa K. Canfield, Erika Giste, Richard Sandstrom, Morgan Diegel, Antony Raubitschek, Hao Wang, Audra K. Johnson, Kristen Lee, Alex Reynolds, Richard Humbert, and John A. Stamatoyannopoulos

Subjects
Multiple Sclerosis, Disease, Regulatory Sequences, Nucleic Acid, Biology, Polymorphism, Single Nucleotide, Article, Fetal Development, Electrocardiography, chemistry.chemical_compound, Fetus, Crohn Disease, Deoxyribonuclease I, Humans, Gene Regulatory Networks, Regulatory Elements, Transcriptional, Allele, Promoter Regions, Genetic, Transcription factor, Alleles, Genetic association, Genetics, Multidisciplinary, Genome, Human, Genetic Variation, DNA, Phenotype, Chromatin, chemistry, Genome-Wide Association Study, Transcription Factors
Abstract

Predictions of Genetic Disease Many genome-wide association studies (GWAS) have identified loci and variants associated with disease, but the ability to predict disease on the basis of these genetic variants remains small. Maurano et al. (p. 1190 ; see the Perspective by Schadt and Chang ; see the cover) characterize the location of GWAS variants in the genome with respect to their proximity to regulatory DNA [marked by deoxyribonuclease I (DNase I) hypersensitive sites] by tissue type, disease, and enrichments in physiologically relevant transcription factor binding sites and networks. They found many noncoding disease associations in regulatory DNA, indicating tissue and developmental-specific regulatory roles for many common genetic variants and thus enabling links to be made between gene regulation and adult-onset disease.

Published
2012
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5. The accessible chromatin landscape of the human genome

Author

Vishwanath R. Iyer, Lingyun Song, Michael O. Dorschner, Joshua M. Akey, Andrew B. Stergachis, Kristen Lee, Anthony Shafer, Shinny Vong, Amartya Sanyal, Hongzhu Qu, Audra K. Johnson, Ericka M. Johnson, Kavita Garg, Minerva E. Sanchez, Daniel Bates, Benjamin Vernot, George Stamatoyannopoulos, Tanya Kutyavin, Robert E. Thurman, Patrick A. Navas, Douglas Dunn, Eric Rynes, Bryan R. Lajoie, Matthew T. Maurano, Jeff Vierstra, Molly Weaver, Jason D. Lieb, Sam John, Alexias Safi, Lisa Boatman, Shane Neph, Zhancheng Zhang, Yongqi Yan, Bum Kyu Lee, Dimitra Lotakis, Zhuzhu Zhang, Gregory E. Crawford, Tristan Frum, Abigail K. Ebersol, Richard Sandstrom, Theresa K. Canfield, Eric Haugen, Erika Giste, Job Dekker, Muneesh Tewari, Alex Reynolds, Eric D. Nguyen, Fidencio Neri, Richard Humbert, Peter J. Sabo, Morgan Diegel, John A. Stamatoyannopoulos, Vaughn Roach, Hao Wang, Rajinder Kaul, Terrence S. Furey, Nathan C. Sheffield, R. Scott Hansen, Jeremy M. Simon, Shamil R. Sunyaev, Boris Lenhard, and Darin London

Subjects
Encyclopedias as Topic, Transcription, Genetic, DNA Footprinting, ATAC-seq, Computational biology, Regulatory Sequences, Nucleic Acid, Biology, DNase-Seq, Article, Evolution, Molecular, 03 medical and health sciences, 0302 clinical medicine, Mutation Rate, Deoxyribonuclease I, Humans, Promoter Regions, Genetic, Enhancer, 030304 developmental biology, Genetics, 0303 health sciences, Multidisciplinary, Genome, Human, Molecular Sequence Annotation, Promoter, DNA, Genomics, DNA Methylation, Chromatin, DNA-Binding Proteins, DNA methylation, Human genome, DNase I hypersensitive site, Transcription Initiation Site, 030217 neurology & neurosurgery, Transcription Factors
Abstract

DNase I hypersensitive sites (DHSs) are markers of regulatory DNA and have underpinned the discovery of all classes of cis-regulatory elements including enhancers, promoters, insulators, silencers and locus control regions. Here we present the first extensive map of human DHSs identified through genome-wide profiling in 125 diverse cell and tissue types. We identify ∼2.9 million DHSs that encompass virtually all known experimentally validated cis-regulatory sequences and expose a vast trove of novel elements, most with highly cell-selective regulation. Annotating these elements using ENCODE data reveals novel relationships between chromatin accessibility, transcription, DNA methylation and regulatory factor occupancy patterns. We connect ∼580,000 distal DHSs with their target promoters, revealing systematic pairing of different classes of distal DHSs and specific promoter types. Patterning of chromatin accessibility at many regulatory regions is organized with dozens to hundreds of co-activated elements, and the transcellular DNase I sensitivity pattern at a given region can predict cell-type-specific functional behaviours. The DHS landscape shows signatures of recent functional evolutionary constraint. However, the DHS compartment in pluripotent and immortalized cells exhibits higher mutation rates than that in highly differentiated cells, exposing an unexpected link between chromatin accessibility, proliferative potential and patterns of human variation. An extensive map of human DNase I hypersensitive sites, markers of regulatory DNA, in 125 diverse cell and tissue types is described; integration of this information with other ENCODE-generated data sets identifies new relationships between chromatin accessibility, transcription, DNA methylation and regulatory factor occupancy patterns. This paper describes the first extensive map of human DNaseI hypersensitive sites — markers of regulatory DNA — in 125 diverse cell and tissue types. Integration of this information with other data sets generated by ENCODE (Encyclopedia of DNA Elements) identified new relationships between chromatin accessibility, transcription, DNA methylation and regulatory-factor occupancy patterns. Evolutionary-conservation analysis revealed signatures of recent functional constraint within DNaseI hypersensitive sites.

Published
2012

6. An expansive human regulatory lexicon encoded in transcription factor footprints

Author

Michael J. MacCoss, Mark Groudine, Molly Weaver, Tanya Kutyavin, John A. Stamatoyannopoulos, Shane Neph, Daniel Bates, Eric Rynes, Benjamin Vernot, Douglas Dunn, Anthony Schafer, Joshua M. Akey, Peter J. Sabo, Jeff Vierstra, Robert E. Thurman, R. Scott Hansen, Andrew B. Stergachis, Rajinder Kaul, Shinny Vong, Alex Reynolds, Theresa K. Canfield, Richard Humbert, Erika Giste, Jun Neri, Michaël Bender, Miaohua Zhang, Kristen Lee, Rachel Byron, Richard Sandstrom, Sam John, Eric Haugen, Gayathri Balasundaram, Vaughn Roach, Morgan Diegel, Hao Wang, Audra K. Johnson, and Matthew T. Maurano

Subjects
Genetics, 0303 health sciences, Multidisciplinary, protein occupancy, DNA footprinting, Promoter, regulation, Computational biology, Biology, DNase-Seq, Article, Conserved sequence, 03 medical and health sciences, 0302 clinical medicine, Regulatory sequence, DNaseI footprinting, DNA methylation, chromatin, Human genome, Transcription factor, 030217 neurology & neurosurgery, 030304 developmental biology, ENCODE
Abstract

Regulatory factor binding to genomic DNA protects the underlying sequence from cleavage by DNase I, leaving nucleotide-resolution footprints. Using genomic DNase I footprinting across 41 diverse cell and tissue types, we detected 45 million transcription factor occupancy events within regulatory regions, representing differential binding to 8.4 million distinct short sequence elements. Here we show that this small genomic sequence compartment, roughly twice the size of the exome, encodes an expansive repertoire of conserved recognition sequences for DNA-binding proteins that nearly doubles the size of the human cis-regulatory lexicon. We find that genetic variants affecting allelic chromatin states are concentrated in footprints, and that these elements are preferentially sheltered from DNA methylation. High-resolution DNase I cleavage patterns mirror nucleotide-level evolutionary conservation and track the crystallographic topography of protein-DNA interfaces, indicating that transcription factor structure has been evolutionarily imprinted on the human genome sequence. We identify a stereotyped 50-base-pair footprint that precisely defines the site of transcript origination within thousands of human promoters. Finally, we describe a large collection of novel regulatory factor recognition motifs that are highly conserved in both sequence and function, and exhibit cell-selective occupancy patterns that closely parallel major regulators of development, differentiation and pluripotency.

Published
2012

7. Genetic Variation at the O-Antigen Biosynthetic Locus in Pseudomonas aeruginosa

Author

Yang Zhou, Arnold Kas, Christopher K. Raymond, James B. Clendenning, David H. Spencer, Rajinder Kaul, Elizabeth H. Sims, Tanya Kutyavin, Maynard V. Olson, and Richard G. Ivey

Subjects
Serotype, Genomics and Proteomics, Molecular Sequence Data, Locus (genetics), Biology, Microbiology, Genome, Homology (biology), DNA sequencing, chemistry.chemical_compound, Bacterial Proteins, Yeasts, Genetic variation, Amino Acid Sequence, Cloning, Molecular, Molecular Biology, Gene, Conserved Sequence, Genetics, Base Sequence, Genetic Variation, O Antigens, chemistry, Pseudomonas aeruginosa, DNA
Abstract

The outer carbohydrate layer, or O antigen, of Pseudomonas aeruginosa varies markedly in different isolates of these bacteria, and at least 20 distinct O-antigen serotypes have been described. Previous studies have indicated that the major enzymes responsible for O-antigen synthesis are encoded in a cluster of genes that occupy a common genetic locus. We used targeted yeast recombinational cloning to isolate this locus from the 20 internationally recognized serotype strains. DNA sequencing of these isolated segments revealed that at least 11 highly divergent gene clusters occupy this region. Homology searches of the encoded protein products indicated that these gene clusters are likely to direct O-antigen biosynthesis. The O15 serotype strains lack functional gene clusters in the region analyzed, suggesting that O-antigen biosynthesis genes for this serotype are harbored in a different portion of the genome. The overall pattern underscores the plasticity of the P. aeruginosa genome, in which a specific site in a well-conserved genomic region can be occupied by any of numerous islands of functionally related DNA with diverse sequences.

Published
2002
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8. A comparative encyclopedia of DNA elements in the mouse genome

Author

Ting Wang, Matthew D. Rasmussen, Dana N. Levasseur, Thomas A. Reh, Fidencio Neri, Tanya Kutyavin, Peter J. Good, Katrina Learned, Kate R. Rosenbloom, Lei Hoon See, Cedric Notredame, Ross C. Hardison, Chris Zaleski, Gerd A. Blobel, Dmitri D. Pervouchine, Shane Neph, Ali Mortazavi, Tamer Kahveci, Arthur I. Skoultchi, Peter J. Sabo, Jorg Drenkow, Alex Reynolds, Rebecca F. Lowdon, Marella F. T. R. de Bruijn, John A. Stamatoyannopoulos, Yin Shen, Richard Humbert, Anthony Kirilusha, Sherman M. Weissman, Roderic Guigó, James Taylor, Paul Flicek, Kristen Lee, Shinny Vong, Xiaoyi Cao, Douglas Dunn, Alessandra Breschi, Elise A. Feingold, Michael A. Beer, Piper M. Treuting, Igor Antoshechkin, Thomas R. Gingeras, Georgi K. Marinov, Tyrone Ryba, Jin Lian, Christine M. Disteche, Javier Herrero, Eric Rynes, Sheng Zhong, Weisheng Wu, Richard Sandstrom, Gilberto DeSalvo, Michael Snyder, Meagan Fastuca, Miguel Pignatelli, Mark Groudine, Sarah Djebali, Nergiz Dogan, Rajinder Kaul, Giovanni Bussotti, Henry Amrhein, Daniel Bates, Matthew S. Wilken, Alexander Dobin, Manolis Kellis, Licia Selleri, Diane Trout, Morgan Diegel, David M. Gilbert, Zhihai Ma, Jeff Vierstra, Xiao Qiao Zhou, Theresa K. Canfield, Venkat S. Malladi, Zhen Ye, Anthony Shafer, Tejaswini Mishra, Yiing Lin, Samantha Kuan, Anshul Kundaje, Thalia Papayannopoulou, Pablo Prieto, Robert E. Thurman, Long Pham, Cricket A. Sloan, Olgert Denas, Kathryn Beal, Erika Giste, Andrea Tanzer, Katherine I. Fisher-Aylor, Shin Lin, M. A. Bender, Stuart H. Orkin, Carrie A. Davis, Benjamin D. Pope, Rachel Byron, Srikanta Gosh, Beatriz Lacerda de Sousa, R. Scott Hansen, Brian A. Williams, Yong Cheng, Kanwei Li, Dongwon Lee, Yanli Wang, Evan E. Eichler, Camden Jansen, Feng Yue, Deepti Jain, Miaohua Zhang, David McCleary, W. James Kent, Melissa S. Cline, Kai Hsin Chang, Leslie B. Adams, Robert S. Harris, Ghia Euskirchen, Christapher S. Morrissey, Alexander Y. Rudensky, Philip Cayting, Drew T. Erickson, Eric Haugen, Michael J. Pazin, Vanessa M. Kirkup, Yi-Chieh Wu, Trupti Kawli, Mukul S. Bansal, Cheryl A. Keller, Lee Edsall, Robert M. Samstein, Bing Ren, Miguel Santos, Steven Z. Josefowicz, Barbara J. Wold, Julien Lagarde, Alan P. Boyle, Mitchell J. Weiss, Audra K. Johnson, Massachusetts Institute of Technology. Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science, Wu, Yi-Chieh, Rasmussen, Matthew D., Bansal, Mukul S., and Kellis, Manolis

Subjects
Epigenomics, DNA Replication, Biology, Regulatory Sequences, Nucleic Acid, ENCODE, Genome, Article, Mice, Species Specificity, Animals, Deoxyribonuclease I, Humans, Cell Lineage, Gene Regulatory Networks, Scaffold/matrix attachment region, Gene, ChIA-PET, Conserved Sequence, Genetics, Multidisciplinary, Mouse genome, Molecular Sequence Annotation, Genomics, Chromatin, Gene Expression Regulation, RNA, Human genome, Transcriptome, Genome-Wide Association Study, Transcription Factors
Abstract

The laboratory mouse shares the majority of its protein-coding genes with humans, making it the premier model organism in biomedical research, yet the two mammals differ in significant ways. To gain greater insights into both shared and species-specific transcriptional and cellular regulatory programs in the mouse, the Mouse ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding, chromatin modifications and replication domains throughout the mouse genome in diverse cell and tissue types. By comparing with the human genome, we not only confirm substantial conservation in the newly annotated potential functional sequences, but also find a large degree of divergence of sequences involved in transcriptional regulation, chromatin state and higher order chromatin organization. Our results illuminate the wide range of evolutionary forces acting on genes and their regulatory regions, and provide a general resource for research into mammalian biology and mechanisms of human diseases. This work is funded by grants R01HG003991 (B.R.), 1U54HG007004 (T.R.G.), 3RC2HG005602 (M.P.S.), GM083337 and GM085354 (D.M.G.), F31CA165863 (B.D.P.), RC2HG005573 and R01DK065806 (R.C.H.) from the National Institutes of Health, and BIO2011-26205 from the Spanish Plan Nacional and ERC 294653 (to R.G.). J.V. is supported by a National Science Foundation Graduate Research Fellowship under grant no. DGE-071824. K.B., M.P., J.H. and P.F. acknowledge the Wellcome Trust (grant number 095908), the NHGRI (grant number U01HG004695) and the European Molecular Biology Laboratory. We thank G. Hon for helping the analysis of high-throughput enhancer validation. L.S. is supported by R01HD043997-09. S.L. was supported by grants F32HL110473 and K99HL119617.

Published
2014

9. Widespread Site-Dependent Buffering of Human Regulatory Polymorphism

Author

Hao-Hao Wang, John A. Stamatoyannopoulos, Tanya Kutyavin, and Matthew T. Maurano

Subjects
Cancer Research, Genome evolution, lcsh:QH426-470, Context (language use), Biology, 03 medical and health sciences, 0302 clinical medicine, Recognition sequence, Genetic variation, Genetics, Genetic variability, Allele, Molecular Biology, Genetics (clinical), Ecology, Evolution, Behavior and Systematics, 030304 developmental biology, 0303 health sciences, Genomics, lcsh:Genetics, CTCF, Evolutionary biology, Functional genomics, 030217 neurology & neurosurgery, Research Article
Abstract

The average individual is expected to harbor thousands of variants within non-coding genomic regions involved in gene regulation. However, it is currently not possible to interpret reliably the functional consequences of genetic variation within any given transcription factor recognition sequence. To address this, we comprehensively analyzed heritable genome-wide binding patterns of a major sequence-specific regulator (CTCF) in relation to genetic variability in binding site sequences across a multi-generational pedigree. We localized and quantified CTCF occupancy by ChIP-seq in 12 related and unrelated individuals spanning three generations, followed by comprehensive targeted resequencing of the entire CTCF–binding landscape across all individuals. We identified hundreds of variants with reproducible quantitative effects on CTCF occupancy (both positive and negative). While these effects paralleled protein–DNA recognition energetics when averaged, they were extensively buffered by striking local context dependencies. In the significant majority of cases buffering was complete, resulting in silent variants spanning every position within the DNA recognition interface irrespective of level of binding energy or evolutionary constraint. The prevalence of complex partial or complete buffering effects severely constrained the ability to predict reliably the impact of variation within any given binding site instance. Surprisingly, 40% of variants that increased CTCF occupancy occurred at positions of human–chimp divergence, challenging the expectation that the vast majority of functional regulatory variants should be deleterious. Our results suggest that, even in the presence of “perfect” genetic information afforded by resequencing and parallel studies in multiple related individuals, genomic site-specific prediction of the consequences of individual variation in regulatory DNA will require systematic coupling with empirical functional genomic measurements., Author Summary A comprehensive understanding of the contribution of individual genome sequences to disease and quantitative traits will require the general ability to predict consequences of genetic variation in non-protein-coding regions, particularly those involved in gene regulation. Here we tested the power to predict such consequences when presented with “complete” information encompassing the genomic DNA binding site patterns of a well-studied regulatory protein across multiple related individuals, coupled with all individual genome sequences at the binding positions. We find that, while there is reasonable ability to predict the average effects of variation within the consensus recognition sequence of a transcriptional regulator, it is not possible to determine reliably the consequences of variation at any given genomic instance. This suggests that the interpretation of individual genome sequences will require comprehensive complementation with functional genomic studies.

Published
2012

10. A User's Guide to the Encyclopedia of DNA Elements (ENCODE)

Author

Zhi Lu, Giltae Song, Troy W. Whitfield, Vishwanath R. Iyer, Teresa Vales, Angelika Merkel, Max Libbrecht, David Haussler, Ting Wang, Kristen Lee, Lingyun Song, Richard M. Myers, Alfonso Valencia, Rachel A. Harte, Xiaoqin Xu, Lucas D. Ward, Hazuki Takahashi, Nathan C. Sheffield, Thomas Derrien, Georgi K. Marinov, Eric D. Nguyen, Bernard B. Suh, Brian J. Raney, Richard Sandstrom, Thomas D. Tullius, Benoit Miotto, Alexander Dobin, Youhan Xu, Lukas Habegger, Ian Dunham, Brian A. Risk, Paul G. Giresi, Morgan C. Giddings, Hualin Xi, Anshul Kundaje, Robert S. Harris, Devin Absher, Peter J. Bickel, Yanbao Yu, Browen Aken, Colin Kingswood, Bryan R. Lajoie, Peter J. Good, Katrina Learned, Laura Elnitski, Shirley Pepke, Brandon King, Piero Carninci, Xinqiong Yang, Ghia Euskirchen, Kathryn Beal, Christelle Borel, Michael Muratet, Robert L. Grossman, David G. Knowles, Zarmik Moqtaderi, Veronika Boychenko, Steven P. Wilder, Michael L. Tress, Florencia Pauli, Alan P. Boyle, Andrea Tanzer, Philipp Kapranov, Serafim Batzoglou, Audra K. Johnson, Jun Neri, Nitin Bhardwaj, Elise A. Feingold, Venkat S. Malladi, Michael M. Hoffman, William Stafford Noble, Andrea Sboner, Mark Gerstein, Stephanie L. Parker, Jacqueline Dumais, Felix Schlesinger, Deborah R. Winter, Randall H. Brown, Thanh Truong, Rebecca F. Lowdon, Paolo Ribeca, Brooke Rhead, Peggy J. Farnham, Krista Thibeault, Terrence S. Furey, Donna Karolchik, Alec Victorsen, Xiaoan Ruan, Rehab F. Abdelhamid, Amy S. Nesmith, Jing Wang, Nicholas M. Luscombe, Alina R. Cao, Diane Trout, Teri Slifer, Peter E. Newburger, Cricket A. Sloan, Dimitra Lotakis, Stephen M. J. Searle, Ali Mortazavi, Alexandra Bignell, Alex Reynolds, Orion J. Buske, Chris Zaleski, Theresa K. Canfield, Ian Bell, Jin Lian, Vanessa K. Swing, Katalin Toth Fejes, Catherine Ucla, Robert E. Thurman, Jacqueline Chrast, Wei Lin, Tim Hubbard, Gary Saunders, Minyi Shi, Vihra Sotirova, Sherman M. Weissman, Jason D. Lieb, Richard Humbert, Kevin M. Bowling, Assaf Gordon, Tarjei S. Mikkelsen, Jing Leng, Thomas R. Gingeras, Fabian Grubert, Nader Jameel, Jost Vielmetter, Hannah Monahan, Preti Jain, Lindsay L. Waite, Tony Shafer, Joel Rozowsky, Michael Coyne, Brian Reed, M. Kay, Harsha P. Gunawardena, Ross C. Hardison, Gavin Sherlock, Alexandra Charos, Joseph D. Fleming, Ann S. Zweig, Jason Gertz, Rajinder Kaul, Xianjun Dong, Alexandre Reymond, Carrie A. Davis, Haiyan Huang, Chao Cheng, Marco Mariotti, Phil Lacroute, Jason A. Dilocker, Kenneth McCue, R. Robilotto, Stylianos E. Antonarakis, Sridar V. Chittur, Justin Jee, Barbara J. Wold, Sudipto K. Chakrabortty, Erica Dumais, Amartya Sanyal, Nathan Boley, Tianyuan Wang, Julien Lagarde, Anthony Kirilusha, Jonathan B. Preall, Kevin Roberts, Erika Giste, Hugo Y. K. Lam, Alvis Brazma, Gregory J. Hannon, Eric Rynes, Philippe Batut, Kevin Struhl, Margus Lukk, Manching Ku, Suganthi Balasubramanian, Sonali Jha, Jorg Drenkow, W. James Kent, Michael Snyder, Jie Wang, Anna Battenhouse, Charles B. Epstein, Rami Rauch, Christopher Shestak, John A. Stamatoyannopoulos, Gaurab Mukherjee, Cédric Howald, Tanya Kutyavin, Huaien Wang, Scott A. Tenenbaum, Wan Ting Poh, Kate R. Rosenbloom, Manolis Kellis, Pauline A. Fujita, Linfeng Wu, Anita Bansal, Molly Weaver, Linda L. Grasfeder, Peter J. Sabo, Qiang Li, Melissa S. Cline, Robert M. Kuhn, Darin London, Seth Frietze, Atif Shahab, Shane Neph, Damian Keefe, James B. Brown, Mark Diekhans, Webb Miller, Katherine Aylor Fisher, Jiang Du, Hadar H. Sheffer, Sarah Djebali, Frank Doyle, Nathan Lamarre-Vincent, Chia-Lin Wei, Laura A.L. Dillon, Jennifer Harrow, Robert C. Altshuler, Tyler Alioto, Raymond K. Auerbach, Adam Frankish, Rebekka O. Sprouse, Patrick J. Collins, E. Christopher Partridge, Zheng Liu, Yoichiro Shibata, Elliott H. Margulies, Abigail K. Ebersol, Kimberly A. Showers, Eric D. Green, Krishna M. Roskin, Job Dekker, Barbara N. Pusey, Ekta Khurana, Gilberto DeSalvo, Yijun Ruan, Hao Wang, Jainab Khatun, Henriette O'Geen, Alexej Abyzov, Brian Williams, Ryan M. McDaniell, Maya Kasowski, Manoj Hariharan, Felix Kokocinski, Gloria Despacio-Reyes, Zhancheng Zhang, Subhradip Karmakar, Ewan Birney, Koon-Kiu Yan, Xian Chen, Shinny Vong, Daniel Sobral, Nick Bild, Seul K.C. Kim, Timo Lassmann, Li Wang, Minerva E. Sanchez, Vaughan Roach, Theodore Gibson, Stephen C. J. Parker, Michael F. Lin, Patrick A. Navas, Laurence R. Meyer, Luiz O. F. Penalva, Bradley E. Bernstein, Kevin P. White, Emilie Aït Yahya Graison, Juan M. Vaquerizas, Sushma Iyengar, Kimberly M. Newberry, Akshay Bhinge, Xiaolan Zhang, Kim Bell, Yoshihide Hayashizaki, Lucas Lochovsky, Noam Shoresh, Hagen Tilgner, Philip Cayting, Dorrelyn Patacsil, Timothy E. Reddy, Eric Haugen, Katherine E. Varley, M. van Baren, Nathan D. Trinklein, Bum Kyu Lee, Tristan Frum, Marianne Lindahl-Allen, Timothy Durham, Roderic Guigó, Christopher W. Maier, Micha Sammeth, Debasish Raha, Timothy R. Dreszer, Benedict Paten, Robbyn Issner, Michael R. Brent, Kevin Y. Yip, Kim Blahnik, Jason Ernst, Zhiping Weng, Henry Amrhein, Arend Sidow, Javier Herrero, Hui Gao, Stephen G. Landt, Pouya Kheradpour, Galt P. Barber, Gregory E. 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Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology. Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology. Department of Physics, Kellis, Manolis, Epstein, Charles B., Bernstein, Bradley E., Shoresh, Noam, Ernst, Jason, Mikkelsen, Tarjei Sigurd, Kheradpour, Pouya, Zhang, Xiaolan, Wang, Li, Issner, Robbyn, Coyne, Michael J., Durham, Timothy, Ku, Manching, Truong, Thanh, Ward, Lucas D., Altshuler, Robert Charles, Lin, Michael F., ENCODE Project Consortium, Antonarakis, Stylianos, and Miotto, Benoit

Subjects
RNA, Messenger/genetics, [SDV]Life Sciences [q-bio], Messenger, Genoma humà, Genome, Medical and Health Sciences, 0302 clinical medicine, Models, ddc:576.5, Biology (General), Conserved Sequence, Genetics, 0303 health sciences, General Neuroscience, RNA-Binding Proteins, Genomics, Biological Sciences, Chromatin, 3. Good health, [SDV] Life Sciences [q-bio], DNA-Binding Proteins, Gene Components, 030220 oncology & carcinogenesis, DNA methylation, Encyclopedia, HIV/AIDS, Proteïnes de la sang -- Aspectes genètics, General Agricultural and Biological Sciences, Databases, Nucleic Acid, Human, Research Article, Quality Control, Process (engineering), QH301-705.5, 1.1 Normal biological development and functioning, Computational biology, Biology, ENCODE, General Biochemistry, Genetics and Molecular Biology, Chromatin/metabolism, Vaccine Related, 03 medical and health sciences, Databases, Genetic, Underpinning research, Humans, RNA, Messenger, RNA-Binding Proteins/genetics/metabolism, Vaccine Related (AIDS), Gene, 030304 developmental biology, Internet, General Immunology and Microbiology, Nucleic Acid, Agricultural and Veterinary Sciences, Base Sequence, Models, Genetic, Genome, Human, Prevention, Human Genome, Computational Biology, DNA Methylation, ENCODE Project Consortium, Gene Expression Regulation, DNA-Binding Proteins/genetics/metabolism, RNA, Human genome, Immunization, Generic health relevance, Developmental Biology
Abstract

The mission of the Encyclopedia of DNA Elements (ENCODE) Project is to enable the scientific and medical communities to interpret the human genome sequence and apply it to understand human biology and improve health. The ENCODE Consortium is integrating multiple technologies and approaches in a collective effort to discover and define the functional elements encoded in the human genome, including genes, transcripts, and transcriptional regulatory regions, together with their attendant chromatin states and DNA methylation patterns. In the process, standards to ensure high-quality data have been implemented, and novel algorithms have been developed to facilitate analysis. Data and derived results are made available through a freely accessible database. Here we provide an overview of the project and the resources it is generating and illustrate the application of ENCODE data to interpret the human genome., National Human Genome Research Institute (U.S.), National Institutes of Health (U.S.)

Published
2011
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