Relevant bibliographies by topics / Epigenomic regulators

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Epigenomic regulators'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Epigenomic regulators"

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Al-Janabi, Ismail. "Therapeutic Targeting of the Regulators of Cancer Epigenomes." Al-Rafidain Journal of Medical Sciences ( ISSN 2789-3219 ) 5 (July 1, 2023): 1–13. http://dx.doi.org/10.54133/ajms.v5i.128.

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Aim: To assess the value of targeting the various molecules that regulate the epigenome in the management of cancer. Method: Peer-reviewed articles were examined in PubMed, Google Scholar, and ResearchGate search tools using keywords given in the manuscript. Main points: Three major epigenomic modifications, namely DNA methylation, histone methylation, and histone acetylation, attracted the most research interest and led to a few globally approved drugs for the treatment of various malignancies. The DNA methylation profiles of cancer have been successfully employed in many aspects of the management of this disease. Conclusion: Epigenomic profiling of cancer specimens has already been successfully employed in the management of cancer in a handful of specialized clinics, and this application could be extended further following more in-depth investigations in this field.
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Paul, Aswathy Mary, Madhavan Radhakrishna Pillai, and Rakesh Kumar. "Prognostic Significance of Dysregulated Epigenomic and Chromatin Modifiers in Cervical Cancer." Cells 10, no. 10 (2021): 2665. http://dx.doi.org/10.3390/cells10102665.

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To broaden the understanding of the epigenomic and chromatin regulation of cervical cancer, we examined the status and significance of a set of epigenomic and chromatin modifiers in cervical cancer using computational biology. We observed that 61 of 917 epigenomic and/or chromatin regulators are differentially upregulated in human cancer, including 25 upregulated in invasive squamous cell carcinomas and 29 in cervical intraepithelial neoplasia 3 (CIN3), of which 14 are upregulated in cervical intraepithelial neoplasia 2 (CIN2). Interestingly, 57 of such regulators are uniquely upregulated in cervical cancer, but not ovarian and endometrial cancers. The observed overexpression of 57 regulators was found to have a prognostic significance in cervical cancer. The collective overexpression of these regulators, as well as its subsets belonging to specific histone modifications and corresponding top ten positively co-overexpressed genes, correlated with reduced survival of patients with high expressions of the tested overexpressed regulators compared to cases with low expressions. Using cell-dependency datasets from human cervical cancer cells, we found that 20 out of 57 epigenomic and chromatin regulators studied here appeared to be essential genes, as the depletion of these genes was accompanied by the loss in cellular viability. In brief, the results presented here provide further insights into the role of epigenomic and chromatin regulators in the oncobiology of cervical cancer and broaden the list of new potential molecules of therapeutic importance.
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Schmitz, Ulf, Jaynish S. Shah, Bijay P. Dhungel, et al. "Widespread Aberrant Alternative Splicing despite Molecular Remission in Chronic Myeloid Leukaemia Patients." Cancers 12, no. 12 (2020): 3738. http://dx.doi.org/10.3390/cancers12123738.

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Vast transcriptomics and epigenomics changes are characteristic of human cancers, including leukaemia. At remission, we assume that these changes normalise so that omics-profiles resemble those of healthy individuals. However, an in-depth transcriptomic and epigenomic analysis of cancer remission has not been undertaken. A striking exemplar of targeted remission induction occurs in chronic myeloid leukaemia (CML) following tyrosine kinase inhibitor (TKI) therapy. Using RNA sequencing and whole-genome bisulfite sequencing, we profiled samples from chronic-phase CML patients at diagnosis and remission and compared these to healthy donors. Remarkably, our analyses revealed that abnormal splicing distinguishes remission samples from normal controls. This phenomenon is independent of the TKI drug used and in striking contrast to the normalisation of gene expression and DNA methylation patterns. Most remarkable are the high intron retention (IR) levels that even exceed those observed in the diagnosis samples. Increased IR affects cell cycle regulators at diagnosis and splicing regulators at remission. We show that aberrant splicing in CML is associated with reduced expression of specific splicing factors, histone modifications and reduced DNA methylation. Our results provide novel insights into the changing transcriptomic and epigenomic landscapes of CML patients during remission. The conceptually unanticipated observation of widespread aberrant alternative splicing after remission induction warrants further exploration. These results have broad implications for studying CML relapse and treating minimal residual disease.
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Zhou, Huaijun. "97 Dissection of Evolution of Cis-Regulatory Elements and Its Application on Genetic Control of Complex Traits in Farm Animals." Journal of Animal Science 101, Supplement_3 (2023): 51–52. http://dx.doi.org/10.1093/jas/skad281.063.

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Abstract Functional Annotation of Animal Genomes (FAANG) has made significant progress on the improvement of the annotation of the functional elements, particularly non-coding regions in farm animal genomes. Different epigenomes including ChIP-seq for 4 histone marks, ATAC-seq, CTCF-seq, RNA-seq, and Hi-C across different tissues in different animal species were generated. Thousands of cis-regulatory elements including promoters and enhancers across different tissues in different species were identified and annotated. A comprehensive characterization and comparison of cis-regulatory elements across tissues and species can help us understand the genetic and evolutionary basis of complex phenotypes. Yet, attempts to dissect the evolution of regulatory elements have generally been small, both regarding the number of tissues and species compared. We demonstrate that genomic variants associated with complex traits and adaptive evolution in farm animals are significantly enriched in active promoters and enhancers. Further analysis suggests that the regulators were significantly enriched in evolutionary breakpoint regions (EBRs) in a tissue-specific and regulator-specific manner. Furthermore, we reveal distinct tissue-specific regulatory elements play important roles in domestication processes. Finally, we provide biological insights on tissue-specific regulatory conservation, and by integrating genome-wide association studies on complex traits, we demonstrate that comparative epigenomic analysis enhances our interpretations of complex traits variations in farm animals and provides novel insights on the role of regulatory elements on the functional conservation across species.
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Tseng, Yen-Tzu, Hung-Fu Liao, Chih-Yun Yu, Chu-Fan Mo, and Shau-Ping Lin. "Epigenetic factors in the regulation of prospermatogonia and spermatogonial stem cells." REPRODUCTION 150, no. 3 (2015): R77—R91. http://dx.doi.org/10.1530/rep-14-0679.

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Appropriate regulation of epigenome within cells is crucial for the determination of cell fate and contributes to the lifelong maintenance of tissue homeostasis. Epigenomic re-establishment during embryonic prospermatogonia development and fine-tune of the epigenetic landscape in postnatal spermatogonial stem cells (SSCs) are two key processes required for functional male germ cell formation. Repression of re-activated transposons and male germline-specific epigenome establishment occur in prospermatogonia, whereas modulations of the epigenetic landscape is important for SSC self-renewal and differentiation to maintain the stem cell pool and support long-term sperm production. Here, we describe the impact of epigenome-related regulators and small non-coding RNAs as well as the influence of epigenome modifications that result from extrinsic signaling for controlling the decision between self-renewal, differentiation and survival in mouse prospermatogonia and SSCs. This article provides a review of epigenome-related molecules involved in cell fate determination in male germ cells and discusses the intriguing questions that arise from these studies.
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Deng, Xian, Xianwei Song, Liya Wei, Chunyan Liu, and Xiaofeng Cao. "Epigenetic regulation and epigenomic landscape in rice." National Science Review 3, no. 3 (2016): 309–27. http://dx.doi.org/10.1093/nsr/nww042.

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Abstract Epigenetic regulation has been implicated in the control of complex agronomic traits in rice (Oryza sativa), a staple food crop and model monocot plant. Recent advances in high-throughput sequencing and the moderately complex genome of rice have made it possible to study epigenetic regulation in rice on a genome-wide scale. This review discusses recent advances in our understanding of epigenetic regulation in rice, with an emphasis on the roles of key epigenetic regulators, the epigenomic landscape, epigenetic variation, transposon repression, and plant development.
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Rada-Iglesias, Alvaro, Ruchi Bajpai, Sara Prescott, Samantha A. Brugmann, Tomek Swigut, and Joanna Wysocka. "Epigenomic Annotation of Enhancers Predicts Transcriptional Regulators of Human Neural Crest." Cell Stem Cell 11, no. 5 (2012): 633–48. http://dx.doi.org/10.1016/j.stem.2012.07.006.

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Smetanina, Mariya A., Valeria A. Korolenya, Alexander E. Kel, et al. "Epigenome-Wide Changes in the Cell Layers of the Vein Wall When Exposing the Venous Endothelium to Oscillatory Shear Stress." Epigenomes 7, no. 1 (2023): 8. http://dx.doi.org/10.3390/epigenomes7010008.

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Epigenomic changes in the venous cells exerted by oscillatory shear stress towards the endothelium may result in consolidation of gene expression alterations upon vein wall remodeling during varicose transformation. We aimed to reveal such epigenome-wide methylation changes. Primary culture cells were obtained from non-varicose vein segments left after surgery of 3 patients by growing the cells in selective media after magnetic immunosorting. Endothelial cells were either exposed to oscillatory shear stress or left at the static condition. Then, other cell types were treated with preconditioned media from the adjacent layer’s cells. DNA isolated from the harvested cells was subjected to epigenome-wide study using Illumina microarrays followed by data analysis with GenomeStudio (Illumina), Excel (Microsoft), and Genome Enhancer (geneXplain) software packages. Differential (hypo-/hyper-) methylation was revealed for each cell layer’s DNA. The most targetable master regulators controlling the activity of certain transcription factors regulating the genes near the differentially methylated sites appeared to be the following: (1) HGS, PDGFB, and AR for endothelial cells; (2) HGS, CDH2, SPRY2, SMAD2, ZFYVE9, and P2RY1 for smooth muscle cells; and (3) WWOX, F8, IGF2R, NFKB1, RELA, SOCS1, and FXN for fibroblasts. Some of the identified master regulators may serve as promising druggable targets for treating varicose veins in the future.
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Boix, Carles A., Benjamin T. James, Yongjin P. Park, Wouter Meuleman, and Manolis Kellis. "Regulatory genomic circuitry of human disease loci by integrative epigenomics." Nature 590, no. 7845 (2021): 300–307. http://dx.doi.org/10.1038/s41586-020-03145-z.

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AbstractAnnotating the molecular basis of human disease remains an unsolved challenge, as 93% of disease loci are non-coding and gene-regulatory annotations are highly incomplete1–3. Here we present EpiMap, a compendium comprising 10,000 epigenomic maps across 800 samples, which we used to define chromatin states, high-resolution enhancers, enhancer modules, upstream regulators and downstream target genes. We used this resource to annotate 30,000 genetic loci that were associated with 540 traits4, predicting trait-relevant tissues, putative causal nucleotide variants in enriched tissue enhancers and candidate tissue-specific target genes for each. We partitioned multifactorial traits into tissue-specific contributing factors with distinct functional enrichments and disease comorbidity patterns, and revealed both single-factor monotropic and multifactor pleiotropic loci. Top-scoring loci frequently had multiple predicted driver variants, converging through multiple enhancers with a common target gene, multiple genes in common tissues, or multiple genes and multiple tissues, indicating extensive pleiotropy. Our results demonstrate the importance of dense, rich, high-resolution epigenomic annotations for the investigation of complex traits.
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kong, ranran, Ayushi S. Patel, Takashi Sato, et al. "Abstract 5709: Transcriptional circuitry of NKX2-1 and SOX1 defines a previously unrecognized lineage subtype of small cell lung cancer." Cancer Research 82, no. 12_Supplement (2022): 5709. http://dx.doi.org/10.1158/1538-7445.am2022-5709.

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Abstract Introduction: The current molecular classification of small cell lung cancer (SCLC) based on expression of four lineage transcription factors, SCLC-A (ASCL1), SCLC-N (NEUROD1), SCLC-P (POU2F3), and SCLC-Y (YAP1) still leaves its major subtype SCLC-A as a large heterogeneous group, necessitating more precise characterization of lineage subclasses. Experimental procedure: To refine the current SCLC classification and to identify specific lineage features of the SCLC subtypes, we performed unsupervised hierarchical clustering of H3K27ac profiles on transcriptional regulators from 25 SCLC cell lines and determined the epigenomic features for each cluster. Functional significance of the transcriptional lineage regulators for the identified cluster was evaluated by cell growth, apoptosis and xenograft using CRISPR-Cas9-mediated deletion. The specific cistromic profiles by ChIP-seq and its functional transcriptional partners using co-immunoprecipitation followed by mass spectrometry were determined to reveal their functional output in the identified subtype. Rb1fl/flTrp53fl/fl and Rb1fl/flTrp53fl/flNkx2-1fl/fl genetic engineered mouse model were generated to explore the function of Nkx2-1 in tumor initiation and differentiation. H3K27ac profiles were further analyzed to reveal 6 human SCLC specimen and 20 mice tumors epigenomic landscapes. Summary: We identified previously uncharacterized epigenomic sub-clusters of the major SCLC-A subtype, named SCLC-A1 and SCLC-A2. SCLC-A1 was characterized by the presence of a super-enhancer at the NKX2-1 locus, which was observed in human SCLC specimens and a murine SCLC model. We found NKX2-1, a dual lung and neural lineage factor, is uniquely relevant in SCLC-A1, where it maintains neural lineage rather than pulmonary epithelial identity. We further found maintenance of this neural identity in SCLC-A1 is mediated by collaborative transcriptional activity with another neuronal transcriptional factor SOX1. ? Conclusions: We comprehensively describe an additional epigenomic heterogeneity of the major SCLC-A subtype, and define SCLC-A1 subtype by the core regulatory circuitry representing NKX2-1 and SOX1 super-enhancers and their functional collaborations to maintain a neuronal linage state. Citation Format: ranran kong, Ayushi S. Patel, Takashi Sato, Seungyeul Yoo, Abhilasha Sinha, Yang Tian, Feng Jiang, Charles A. Powell, Eric Snyder, Jiantao Jiang, Shaomin Li, Hideo Watanabe. Transcriptional circuitry of NKX2-1 and SOX1 defines a previously unrecognized lineage subtype of small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5709.
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Dissertations / Theses on the topic "Epigenomic regulators"

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Ferré, Quentin. "Leveraging combinations of epigenomic regulators." Electronic Thesis or Diss., Aix-Marseille, 2021. http://www.theses.fr/2021AIXM0151.

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A régulation cis-génomique chez l’homme est effectuée par des régulateurs de la chromatine, tels que les marques d’histones et les régulateurs de transcription (TR). Ils fonctionnent rarement seuls, mais plutôt en complexes. Le développement du séquençage NGS fournit des méthodes pour étudier cette régulation, incluant le ChIP-seq. Le but de cette thèse est de tirer parti de ces combinaisons avec des méthodes d’apprentissage automatique, efficaces pour apprendre les régularités dans les données. Nous représentons les régions d’intérêt sous forme de listes d’intervalles, converties en représentations matricielles et tensorielles. De fait, nos approches sont généralisables à toute liste d’intervalles. Le ChIP-seq peut souffrir d’erreurs et de faux positifs, d’un contrôle de qualité médiocre, etc. Ces biais sont difficiles à corriger, et les grands volumes de données augmentent la probabilité d’erreurs. Nous supposons que le bruit ne respectera pas les combinaisons usuelles entre les sources et proposons atyPeak, qui exploite les combinaisons de TR et d’expériences redondantes de ReMap. Nous utilisons un auto-encodeur convolutionnel multi-vues pour une compression "de juste milieu". Nous proposons des approches pour évaluer les auto-encodeurs. Enfin, l’enrichissement de combinaisons n-wise d’éléments (par rapport à ce qui est attendu au hasard) doit être quantifié avec précision. Nous proposons OLOGRAM- MODL, une méthode Monte Carlo ajustant un modèle binomial négatif sur le nombre de paires de bases où elle sont observées. Nous proposons un algorithme d’extraction d’itemsets pour identifier les combinaisons qui reconstruisent le mieux les données d’origine<br>Genetic cis-regulation in humans is effected through chromatin regulators, such as histone marks and Transcriptional Regulators (TRs). Those regulators seldom act alone, instead forming complexes. The development of NGS provides experimental methods to study this regulation, which includes ChIP-seq. The goal of this thesis is to leverage such combinations through the use of machine learning methods, which are effective at learning regularities in the data. We propose to represent the regions where regulators bind as lists of intervals, converted into matrix and tensor representations. ChIP-seq and other experimental assays can suffer from errors and false positives, poor quality control, and several other biases that are difficult to correct. Furthermore, the use of larger volumes of data increases the probability of errors. We assume that noise peaks will not respect the usual combinations between sources, and propose atyPeak which exploits combinations of TRs, and redundant experiments from the ReMap database. We propose to use a multi-view convolutional autoencoder to perform a “Goldilocks” compression. We developed approaches to evaluate autoencoders based on their respect of existing correlations. Finally, the enrichment of given n-wise combinations of elements (how often they are found compared to expected by chance) needs to be precisely quantified. We propose the OLOGRAM-MODL approach, demonstrating a Monte Carlo based method to fit a Negative Binomial model on the number of base pairs on which a given combination is observed. We also propose an itemset mining algorithm to based on which combinations best rebuild the original data
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DAS, VIVEK. "LEVERAGING TRANSCRIPTOMIC ANALYSIS TO IDENTIFY TRANSCRIPTION FACTORS ORCHESTRATING CANCER PROGRESSION." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/559711.

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Next generation sequencing (NGS) technology is currently employed to explore the molecular profiles associated to different biological contexts. The application of this technology provides at same time a high-resolution and global view of the genome and epigenome phenomena, enabling us to study the molecular events underlying many human diseases, including cancer. Our lab tries to exploit the utility of high throughput sequencing technologies generating genomic, transcriptomic and epigenomic data from patient's cohort to study the underlying molecular mechanisms that characterize the specific diseases and map the key regulators that can be critical targets for relevant therapeutic measures. I take the advantage of this technology to mainly understand two aggressive cancers: Ovarian Cancer (OC) and Glioblastoma multiforme (GBM). OC is a leading cause of cancer-related death for which no significant therapeutic progress has been made in the last decades. Also, in this case, despite multimodal treatment its prognosis remains extremely poor. This is due to the fact that the molecular mechanisms underlying OC tumorigenesis and progression are still poorly understood (Vaughan et al., 2011). GBM is the most common and aggressive primary brain malignancy with very poor prognosis (Frattini et al., 2013). The median survival rate is of 12-15 months (Singh et al., 2012) with 5-year survival that is less than 5% despite the multimodal treatment which include surgery, radiotherapy and chemotherapy. To this end, I will be integrating various genomic and transcriptomic analysis to define the key regulatory actors that characterize the disease progression paving. This integrated analysis has been devised in form of a computational workflow that gives way for a discovery pipeline for physiopathologically meaningful epigenetic targets that can lead to therapies.
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Jhanwar, Shalu 1986. "Computational analysis of epigenomic variability and its effect on regulatory activity." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/580601.

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Epigenetics provides a plausible link between the environment and changes in gene expression that might contribute to disease phenotypes. The main goal of the thesis is to study epigenomic variability and their effect on the regulatory activity underlying chromatin dynamics. With an ultimate aim to identify regulatory variants driving cancer as well as disease specific epigenomic patterns in neurological diseases, the thesis deals with the development and subsequent implementation of a novel supervised machine-learning based enhancer predictor (GEP). Further, to address the role of DNA methylation during development of two distinct larval morphs from a single egg in a parasitic polyembryonic wasp, we have developed a novel computational method (dMeth-X) that identifies putative differentially methylated genes responsible for morphological and behavioral differences between the larval forms. Additionally, the thesis focuses on the study of the effect of external factors on the epigenomic variability on the mouse brain cortex. Overall, we believe that my doctoral thesis is a successful endeavor to study the epigenetic variability and regulatory activity using next-generation sequencing approaches.<br>La epigenética proporciona un enlace plausible entre el medio ambiente y los cambios en la expresión de genes que podrían contribuir a fenotipo de las enfermedades. El objetivo principal de la tesis es el estudio de la variabilidad epigenómica y su efecto sobre la actividad reguladora subyacente a la dinámica de la cromatina. Con un objetivo último de identificar variantes de regulación que contribuyen al cáncer, así como patrones epigenómicos específicos en enfermedades neurológicas, las tesis se enfoca en el desarrollo y posterior aplicación de un nuevo método supervisado para predecir potenciadores basado en aprendizaje automático (GEP). Además, para abordar el papel de la metilación del ADN en la configuración de dos formas larvarias distintas de un solo huevo en una avispa poliembriónica parasitaria, hemos desarrollado un nuevo método computacional (dMeth-X) para identificar los genes diferencialmente metilados que podrían contribuir distinguiendo formas larvarias contrastantes. Adicionalmente, la tesis incorporó el estudio del efecto de factores externos sobre la variabilidad epigenómica de la corteza del cerebro de ratón. En general, creemos que mi tesis doctoral es un esfuerzo exitoso para estudiar la variabilidad epigenética y la actividad reguladora utilizando enfoques de secuenciación de próxima generación.
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Jené, i. Sanz Alba 1984. "Integrative study of the regulatory and epigenomic programs involved in cancer development." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/113380.

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El càncer ha estat tradicionalment considerat una malaltia fonamentalment genètica, però recentment s'està fent palès que la desregulació de mecanismes epigenètics contribueix en gran manera al desenvolupament tumoral. Al bell mig de la intersecció entre la genètica i l'epigenètica s'hi troben els factors reguladors de la cromatina (CRFs, en anglès), que són un focus important de recerca a causa de la seva potencial utilitat en teràpies contra el càncer. En aquesta tesi, determino l'estat transcriptòmic de cèl·lules normals i tumorals basant-me en informació epigenètica i regulatòria, i descric l'existència d'una sincronització global de l'expresió gènica en què la regulació controlada per Polycomb es manifesta com a un dels dos components principals. Presento una anàlisi sobre com la baixa expressió dels gens regulats per Polycomb contribueix a l'avenç del càncer de mama i a la transició entre epitel·li i mesènquima. A més, identifico aquesta baixa expressió com a factor valuós de pronòstic independent. Aprofitant les dades genòmiques de càncer que han estat posades a la disposició del públic recentment, també avaluo l'estat mutacional dels CRFs en molts tumors humans provinents de diferents teixits i línies cel·lulars de càncer. Els resultats indiquen que 39 CRFs són potencialment conductors del procès cancerígen en almenys un teixit, malgrat que molts d'ells es torben mutats en freqüències relativament baixes. Finalment, presento un recurs per a visualitzar i analitzar alteracions genòmiques entre línies cel·lulars de càncer en el context de la resistència a fàrmacs i de la informació sobre alteracions de<br>Cancer has traditionally been regarded as a genetic disease, but recently it is becoming apparent that the deregulation of epigenetic mechanisms greatly contributes to tumour development. At the crossing of genetics and epigenetics lie chromatin regulatory factors (CRFs), which are the focus of intense research due to their potential usefulness in anticancer therapy. In this thesis, I determine the transcriptomic state of normal and tumour cells based on epigenetic and regulatory information, and describe the existence of a global synchronisation of gene expression in which Polycomb regulation arises as one of the two main components. I present an analysis on how the under-expression of Polycomb regulated genes contributes to breast cancer progression and epithelial to mesenchymal transition. Furthermore, I identify this under-expression as a valuable independent prognostic factor. Taking advantage on the wealth of cancer genomics data made available recently, I also evaluate the mutational status of CRFs across many human tumours from different tissues and cancer cell lines, and find that 39 CRFs are potential cancer drivers in at least one tissue, even though most of them are mutated at relatively low frequencies. Finally, I present a resource to visualise and analyse genomic alterations across cancer cell lines in the context of drug sensitivity/resistance and the information on somatic tumour alterations.
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Purcaro, Michael J. "Analysis, Visualization, and Machine Learning of Epigenomic Data." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/938.

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The goal of the Encyclopedia of DNA Elements (ENCODE) project has been to characterize all the functional elements of the human genome. These elements include expressed transcripts and genomic regions bound by transcription factors (TFs), occupied by nucleosomes, occupied by nucleosomes with modified histones, or hypersensitive to DNase I cleavage, etc. Chromatin Immunoprecipitation (ChIP-seq) is an experimental technique for detecting TF binding in living cells, and the genomic regions bound by TFs are called ChIP-seq peaks. ENCODE has performed and compiled results from tens of thousands of experiments, including ChIP-seq, DNase, RNA-seq and Hi-C. These efforts have culminated in two web-based resources from our lab—Factorbook and SCREEN—for the exploration of epigenomic data for both human and mouse. Factorbook is a peak-centric resource presenting data such as motif enrichment and histone modification profiles for transcription factor binding sites computed from ENCODE ChIP-seq data. SCREEN provides an encyclopedia of ~2 million regulatory elements, including promoters and enhancers, identified using ENCODE ChIP-seq and DNase data, with an extensive UI for searching and visualization. While we have successfully utilized the thousands of available ENCODE ChIP-seq experiments to build the Encyclopedia and visualizers, we have also struggled with the practical and theoretical inability to assay every possible experiment on every possible biosample under every conceivable biological scenario. We have used machine learning techniques to predict TF binding sites and enhancers location, and demonstrate machine learning is critical to help decipher functional regions of the genome.
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Zhu, Yan. "Microfluidic Technology for Low-Input Epigenomic Analysis." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/83402.

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Epigenetic modifications, such as DNA methylation and histone modifications, play important roles in gene expression and regulation, and are highly involved in cellular processes such as stem cell pluripotency/differentiation and tumorigenesis. Chromatin immunoprecipitation (ChIP) is the technique of choice for examining in vivo DNA-protein interactions and has been a great tool for studying epigenetic mechanisms. However, conventional ChIP assays require millions of cells for tests and are not practical for examination of samples from lab animals and patients. Automated microfluidic chips offer the advantage to handle small sample sizes and facilitate rapid reaction. They also eliminate cumbersome manual handling. In this report, I will talk about three different projects that utilized microfluidic immunoprecipitation followed by next genereation sequencing technologies to enable low input and high through epigenomics profiling. First, I examined RNA polymerase II transcriptional regulation with microfluidic chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) assays. Second, I probed the temporal dynamics in the DNA methylome during cancer development using a transgenic mouse model with microfluidic methylated DNA immunoprecipitation followed by next generation sequencing (MeDIP-seq) assays. Third, I explored negative enrichment of circulating tumor cells (CTCs) followed by microfluidic ChIP-seq technology for studying temporal dynamic histone modification (H3K4me3) of patient-derived tumor xenograft on an immunodeficient mouse model during the course of cancer metastasis. In the first study, I adapted microfluidic ChIP-seq devices to achieve ultrahigh sensitivity to study Pol2 transcriptional regulation from scarce cell samples. I dramatically increased the assay sensitivity to an unprecedented level (~50 K cells for pol2 ChIP-seq). Importantly, this is three orders of magnitude more sensitive than the prevailing pol2 ChIP-seq assays. I showed that MNase digestion provided better ChIP-seq signal than sonication, and two-steps fixation with MNase digestion provided the best ChIP-seq quality followed by one-step fixation with MNase digestion, and lastly, no fixation with MNase digestion. In the second study, I probed dynamic epigenomic changes during tumorigenesis using mice often require profiling epigenomes using a tiny quantity of tissue samples. Conventional epigenomic tests do not support such analysis due to the large amount of materials required by these assays. In this study, I developed an ultrasensitive microfluidics-based methylated DNA immunoprecipitation followed by next-generation sequencing (MeDIP-seq) technology for profiling methylomes using as little as 0.5 ng DNA (or ~100 cells) with 1.5 h on-chip process for immunoprecipitation. This technology enabled me to examine genome-wide DNA methylation in a C3(1)/SV40 T-antigen transgenic mouse model during different stages of mammary cancer development. Using this data, I identified differentially methylated regions and their associated genes in different periods of cancer development. Interestingly, the results showed that methylomic features are dynamic and change with tumor developmental stage. In the last study, I developed a negative enrichment of CTCs followed by ultrasensitive microfluidic ChIP-seq technology for profiling histone modification (H3K4Me3) of CTCs to resolve the technical challenges associated with CTC isolation and difficulties related with tools for profiling whole genome histone modification on tiny cell samples.<br>Ph. D.
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Batra, Rajbir Nath. "Decoding the regulatory role and epiclonal dynamics of DNA methylation in 1482 breast tumours." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/274923.

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Breast cancer is a clinically and molecularly heterogeneous disease displaying distinct therapeutic responses. Although recent studies have explored the genomic and transcriptomic landscapes of breast cancer, the epigenetic architecture has received less attention. To address this, an optimised Reduced Representation Bisulfite Sequencing protocol was performed on 1482 primary breast tumours (and 237 matched adjacent normal tissues). This constitutes the largest breast cancer methylome yet, and this thesis describes the bioinformatics and statistical analysis of this study. Noticeable epigenetic drift (both gain and loss of homogeneous DNA methylation patterns) was observed in breast tumours when compared to normal tissues, with markedly higher differences in late replicating genomic regions. The extent of epigenetic drift was also found to be highly heterogeneous between the breast tumours and was sharply correlated with the tumour’s mitotic index, indicating that epigenetic drift is largely a consequence of the accumulation of passive cell division related errors. A novel algorithm called DMARC (Directed Methylation Altered Regions in Cancer) was developed that utilised the tumour-specific drift rates to discriminate between methylation alterations attained as a consequence of stochastic cell division errors (background) and those reflecting a more instructive biological process (directed). Directed methylation alterations were significantly enriched for gene expression changes in breast cancer, compared to background alterations. Characterising these methylation aberrations with gene expression led to the identification of breast cancer subtype-specific epigenetic genes with consequences on transcription and prognosis. Cancer genes may be deregulated by multiple mechanisms. By integrating with existing copy number and gene expression profiles for these tumours, DNA methylation alterations were revealed as the predominant mechanism correlated with differentially expressed genes in breast cancer. The crucial role of DNA methylation as a mechanism to target the silencing of specific genes within copy number amplifications is also explored which led to the identification of a putative tumour suppressor gene, THSZ2. Finally, the first genome-wide assessment of epigenomic evolution in breast cancer is conducted. Both, the level of intratumoural heterogeneity, and the extent of epiallelic burden were found to be prognostic, and revealed an extraordinary distinction in the role of epiclonal dynamics in different breast cancer subtypes. Collectively, the results presented in this thesis have shed light on the somatic DNA methylation basis of inter-patient as well as intra-tumour heterogeneity in breast cancer. This complements our genetic knowledge of the disease, and will help move us towards tailoring treatments to the patient's molecular profile.
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Bogatyrova, Olga [Verfasser], and Christoph [Akademischer Betreuer] Plass. "Mutations in regulators of the epigenome and their effects on the DNA methylome / Olga Bogatyrova ; Betreuer: Christoph Plass." Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180617304/34.

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Morikawa, Hiromasa. "Differential roles of epigenetic changes and Foxp3 expression in regulatory T cell-specific transcriptional regulation." Kyoto University, 2013. http://hdl.handle.net/2433/180610.

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Floc'hlay, Swann. "Computational analysis and modelling of regulatory networks controlling embryonic development." Electronic Thesis or Diss., Université Paris sciences et lettres, 2020. http://www.theses.fr/2020UPSLE036.

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La formation d’un embryon est dictée par la séquence ADN propre à cet organisme. La variabilité génétique donne naissance à une grande diversité morphologique, tout en maintenant une organisation générale robuste. Les mutations présentes dans les régions cis-régulatrices impactent la transcription via des mécanismes épigénomiques. La variabilité d’expression génique qui en découle peut être compensée par des mécanismes trans de rétrocontrôle au sein du réseau de régulation. L’organisation précise de ces interactions cis et trans restent encore difficile à déchiffrer. Afin de mieux saisir l’effet des mutations sur la transcription, j’ai analysé des données génétiques, épigénomiques et transcriptomiques en collaboration avec le laboratoire Furlong (EMBL, Heidelberg). L’utilisation de données allèle-spécifiques de lignées F1 de Drosophile a permis d’inférer les interactions directes en cis entre les niveaux de régulation, suggérant une différence d’action des marques épigénétiques H3K27ac et H3K4me3 sur l’expression des gènes. Pour mieux comprendre l’impact en trans de la structure des réseaux de régulation sur l’expression génique, j’ai ensuite construit un modèle logique de la spécification de l’axe dorso-ventral chez l’embryon d’oursin, en collaboration avec le laboratoire Lepage (iBV, Nice). Les analyses multicellulaires et stochastiques ont permis de détecter les composants clés du réseau, notamment la dynamique de répression mutuelle entre Nodal et BMP. En conclusion, l’analyse de données allèle-spécifique et la modélisation logique m’ont permis de d’étudier les mécanismes de la régulation transcriptionnelle sous deux perspectives complémentaires<br>The development of an embryo derives from the DNA sequence of this organism. Genetic variability gives rise to great morphological diversity, while maintaining a robust general organisation. Mutations present within cis-regulatory regions impact transcription via epigenomic mechanisms. The resulting variability in gene expression can be buffered by tran feedback mechanisms within the regulatory network. The precise organisation of these cis and trans interactions remains difficult to decipher. In order to better grasp the effect of mutations on transcription, I analysed genetic, epigenomic and transcriptomic data in collaboration with the Furlong laboratory (EMBL, Heidelberg). The use of allele-specific data from Drosophila F1 lines enabled to infer direct cis-interactions between the regulatory layers, suggesting a difference in the action of the epigenomic markers H3K27ac and H3K4me3 on gene expression. To better understand the trans impact of the structure of regulatory networks on gene expression, I have built a logical model of the dorsal-ventral axis specification in sea urchin embryo, in collaboration with the Lepage laboratory (iBV, Nice). Multicellular and stochastic analyses permitted to detect key components of the network, including the cross-repression dynamic between Nodal and BMP. To conclude, allele-specific data analysis and logical modelling allowed me to study the mechanisms of transcription regulation from two complementary perspectives
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Books on the topic "Epigenomic regulators"

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Lusardi, Theresa A., and Detlev Boison. Ketogenic Diet, Adenosine, Epigenetics, and Antiepileptogenesis. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0023.

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Epilepsy is common, affecting about 1% of the population. Conventional treatments are ineffective in about one third of patients, and current therapies do not prevent epilepsy or its progression. For individuals with drug-refractory epilepsy the ketogenic diet (KD) can provide seizure relief in approximately fifty percent of patients, with complete and permanent remission in some cases, suggesting possible antiepileptogenic effects of the diet. Whereas mechanisms underlying antiseizure effects of KD have been identified, mechanistic links between KD therapy and antiepileptogenesis constitute a novel area of research. An adenosine receptor-mediated role of KD therapy in seizure suppression is well established, and recent evidence demonstrates that the KD regulates adenosine homeostasis in the brain. Adenosine in turn has previously unappreciated epigenetic functions as a regulator of DNA methylation. This chapter discusses recent evidence that KD influences the epigenome through modulation of adenosine metabolism as a plausible antiepileptogenic mechanism of the diet.
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Book chapters on the topic "Epigenomic regulators"

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Zhu, Yan, and Chang Lu. "Microfluidic Chromatin Immunoprecipitation for Analysis of Epigenomic Regulations." In Microfluidic Methods for Molecular Biology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30019-1_16.

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Jhanwar, Shalu. "Computational Epigenomics and Its Application in Regulatory Genomics." In Bioinformatics: Sequences, Structures, Phylogeny. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1562-6_6.

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Hu, Yongfeng, and Dao-Xiu Zhou. "Rice Epigenomes: Characteristics, Regulatory Functions, and Reprogramming Mechanisms." In Rice Genomics, Genetics and Breeding. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7461-5_23.

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Roy Choudhury, Samrat, and Brian A. Walker. "Aberrant Epigenomic Regulatory Networks in Multiple Myeloma and Strategies for Their Targeted Reversal." In RNA Technologies. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14792-1_22.

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Klann, Tyler S., Gregory E. Crawford, Timothy E. Reddy, and Charles A. Gersbach. "Screening Regulatory Element Function with CRISPR/Cas9-based Epigenome Editing." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7774-1_25.

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Halene, Tobias B., Gregor Hasler, Amanda Mitchell, and Schahram Akbarian. "Epigenomic Exploration of the Human Brain." In Psychiatric Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190221973.003.0010.

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The exploration of the epigenome has become a flourishing area in the neurosciences. Scientists increasingly appreciate that even the position of genetic material within the nucleus is purposeful, and its spatial orientation conveys information with critical influence on transcription, genome integrity, and stability. Together, epigenetic and three-dimensional genome data hold promise to reveal how DNA variants and mutations come into play in brain disease. Powerful new technologies can now map transcriptome, DNA-methylome, and other epigenetic regulators on the level of single brain cells. Many of these findings are limited to preclinical studies. Nevertheless, the advent of chromatin-modifying drugs in cancer therapy and the discovery that approved medications such as valproic acid and lithium have a chromatin-modifying effect have spurred hopes for improved biological therapies. Here we summarize current concepts and emerging insights into epigenetic regulation, with a focus on human brain and the neurobiology and pharmacology of psychiatric disorders.
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Zhou, Tong. "Small non-coding RNAs as epigenetic regulators." In Nutritional Epigenomics. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816843-1.00003-5.

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Beetch, Megan, Sadaf Harandi-Zadeh, Kate Shen, and Barbara Stefanska. "Stilbenoids as dietary regulators of the cancer epigenome." In Nutritional Epigenomics. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816843-1.00021-7.

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Mihaylova, Maria M., and Matthew S. Stratton. "Short chain fatty acids as epigenetic and metabolic regulators of neurocognitive health and disease." In Nutritional Epigenomics. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816843-1.00023-0.

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Yan, Menghong. "The paternal diet regulates the offspring epigenome and health." In Nutritional Epigenomics. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816843-1.00012-6.

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Conference papers on the topic "Epigenomic regulators"

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Takamatsu, Hironori, Naoko Hattori, Naofumi Asano, et al. "Abstract 843: Epigenomic disruption of adipogenic regulators in dedifferentiated liposarcoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-843.

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Takamatsu, Hironori, Naoko Hattori, Naofumi Asano, et al. "Abstract 843: Epigenomic disruption of adipogenic regulators in dedifferentiated liposarcoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-843.

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GEVAERT, OLIVIER, and SYLVIA PLEVRITIS. "IDENTIFYING MASTER REGULATORS OF CANCER AND THEIR DOWNSTREAM TARGETS BY INTEGRATING GENOMIC AND EPIGENOMIC FEATURES." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814447973_0013.

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Worsham, MJ, KM Chen, I. Datta, JK Stephen, D. Chitale, and G. Divine. "Abstract P1-04-06: Network integration of epigenomic data: Leveraging the concept of master regulators in ER negative breast cancer." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p1-04-06.

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Battle, Stephanie L., Antti Larjo, Joling Liao, Harri Lähdesmäki, Andre Lieber, and R. David Hawkins. "Abstract AS04: Epigenomic characterization of gene regulatory networks in human ovarian cancer stem cells." In Abstracts: 10th Biennial Ovarian Cancer Research Symposium; September 8-9, 2014; Seattle, WA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.ovcasymp14-as04.

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LaFave, Lindsay M., Vinay Kartha, Sai Ma, et al. "Abstract PR08: Leveraging single-cell epigenomics to uncover regulatory programs in lung adenocarcinoma." In Abstracts: AACR Special Conference on the Evolving Landscape of Cancer Modeling; March 2-5, 2020; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.camodels2020-pr08.

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Tricarico, Rossella, Pietro Mancuso, Vikram Bhattacharjee, et al. "Abstract LB-249: TDG, a dual genomic and epigenomic regulator, as a novel antimelanoma target." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-249.

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XU, Liangliang, Feng WU, Otto K. W. CHEUNG, et al. "Abstract 868: Epigenomic profiling of primary hepatocellular carcinoma reveals super-enhancer-associated chromatin regulator network." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-868.

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XU, Liangliang, Feng WU, Otto K. W. CHEUNG, et al. "Abstract 868: Epigenomic profiling of primary hepatocellular carcinoma reveals super-enhancer-associated chromatin regulator network." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-868.

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Zacharias, W., M. Morley, D. T. Swarr, P. Senthamarai Kannan, M. C. Basil, and E. E. Morrisey. "Integrated Epigenomic Analysis of the Gene Regulatory Networks Underlying Regenerative Capacity in Alveolar Epithelial Progenitor Cells." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4012.

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