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Article ; Online: Analysing miRNA-Target Gene Networks in Inflammatory Bowel Disease and Other Complex Diseases Using Transcriptomic Data

John P. Thomas / Marton Ölbei / Johanne Brooks-Warburton / Tamas Korcsmaros / Dezso Modos

Genes, Vol 13, Iss 370, p

2022 Volume 370

Abstract: Patients with inflammatory bowel disease (IBD) are known to have perturbations in microRNA (miRNA) levels as well as altered miRNA regulation. Although experimental methods have provided initial insights into the functional consequences that may arise ... ...

Abstract	Patients with inflammatory bowel disease (IBD) are known to have perturbations in microRNA (miRNA) levels as well as altered miRNA regulation. Although experimental methods have provided initial insights into the functional consequences that may arise due to these changes, researchers are increasingly utilising novel bioinformatics approaches to further dissect the role of miRNAs in IBD. The recent exponential increase in transcriptomics datasets provides an excellent opportunity to further explore the role of miRNAs in IBD pathogenesis. To effectively understand miRNA-target gene interactions from gene expression data, multiple database resources are required, which have become available in recent years. In this technical note, we provide a step-by-step protocol for utilising these state-of-the-art resources, as well as systems biology approaches to understand the role of miRNAs in complex disease pathogenesis. We demonstrate through a case study example how to combine the resulting miRNA-target gene networks with transcriptomics data to find potential disease-specific miRNA regulators and miRNA-target genes in Crohn’s disease. This approach could help to identify miRNAs that may have important disease-modifying effects in IBD and other complex disorders, and facilitate the discovery of novel therapeutic targets.
Keywords	miRNA ; network biology ; ulcerative colitis ; Crohn’s disease ; transcriptomics ; microarrays ; Genetics ; QH426-470
Subject code	610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Sherlock

Matthew Madgwick / David Fazekas / Balazs Bohar / Mate Szalay-Beko / Tamás Korcsmáros / Marton Olbei / Luca Csabai

F1000Research, Vol

an open-source data platform to store, analyze and integrate Big Data for computational biologists [version 3; peer review: 2 approved]

2023 Volume 10

Abstract: In the era of Big Data, data collection underpins biological research more than ever before. In many cases, this can be as time-consuming as the analysis itself. It requires downloading multiple public databases with various data structures, and in ... ...

Abstract	In the era of Big Data, data collection underpins biological research more than ever before. In many cases, this can be as time-consuming as the analysis itself. It requires downloading multiple public databases with various data structures, and in general, spending days preparing the data before answering any biological questions. Here, we introduce Sherlock, an open-source, cloud-based big data platform (https://earlham-sherlock.github.io/) to solve this problem. Sherlock provides a gap-filling way for computational biologists to store, convert, query, share and generate biology data while ultimately streamlining bioinformatics data management. The Sherlock platform offers a simple interface to leverage big data technologies, such as Docker and PrestoDB. Sherlock is designed to enable users to analyze, process, query and extract information from extremely complex and large data sets. Furthermore, Sherlock can handle different structured data (interaction, localization, or genomic sequence) from several sources and convert them to a common optimized storage format, for example, the Optimized Row Columnar (ORC). This format facilitates Sherlock’s ability to quickly and efficiently execute distributed analytical queries on extremely large data files and share datasets between teams. The Sherlock platform is freely available on GitHub, and contains specific loader scripts for structured data sources of genomics, interaction and expression databases. With these loader scripts, users can easily and quickly create and work with specific file formats, such as JavaScript Object Notation (JSON) or ORC. For computational biology and large-scale bioinformatics projects, Sherlock provides an open-source platform empowering data management, analytics, integration and collaboration through modern big data technologies.
Keywords	Software ; Computational biology ; Network biology ; Systems biology ; Data lake ; big data ; eng ; Medicine ; R ; Science ; Q
Subject code	004
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Sherlock

Matthew Madgwick / David Fazekas / Balazs Bohar / Mate Szalay-Beko / Tamás Korcsmáros / Marton Olbei / Luca Csabai

F1000Research, Vol

an open-source data platform to store, analyze and integrate Big Data for computational biologists [version 2; peer review: 2 approved]

2022 Volume 10

Abstract	In the era of Big Data, data collection underpins biological research more than ever before. In many cases, this can be as time-consuming as the analysis itself. It requires downloading multiple public databases with various data structures, and in general, spending days preparing the data before answering any biological questions. Here, we introduce Sherlock, an open-source, cloud-based big data platform (https://earlham-sherlock.github.io/) to solve this problem. Sherlock provides a gap-filling way for computational biologists to store, convert, query, share and generate biology data while ultimately streamlining bioinformatics data management. The Sherlock platform offers a simple interface to leverage big data technologies, such as Docker and PrestoDB. Sherlock is designed to enable users to analyze, process, query and extract information from extremely complex and large data sets. Furthermore, Sherlock can handle different structured data (interaction, localization, or genomic sequence) from several sources and convert them to a common optimized storage format, for example, the Optimized Row Columnar (ORC). This format facilitates Sherlock’s ability to quickly and efficiently execute distributed analytical queries on extremely large data files and share datasets between teams. The Sherlock platform is freely available on GitHub, and contains specific loader scripts for structured data sources of genomics, interaction and expression databases. With these loader scripts, users can easily and quickly create and work with specific file formats, such as JavaScript Object Notation (JSON) or ORC. For computational biology and large-scale bioinformatics projects, Sherlock provides an open-source platform empowering data management, analytics, integration and collaboration through modern big data technologies.
Keywords	Software ; Computational biology ; Network biology ; Systems biology ; Data lake ; big data ; eng ; Medicine ; R ; Science ; Q
Subject code	004
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: ULK1 and ULK2 are less redundant than previously thought

Amanda Demeter / Mari Carmen Romero-Mulero / Luca Csabai / Márton Ölbei / Padhmanand Sudhakar / Wilfried Haerty / Tamás Korcsmáros

Scientific Reports, Vol 10, Iss 1, Pp 1-

computational analysis uncovers distinct regulation and functions of these autophagy induction proteins

2020 Volume 17

Abstract: Abstract Macroautophagy, the degradation of cytoplasmic content by lysosomal fusion, is an evolutionary conserved process promoting homeostasis and intracellular defence. Macroautophagy is initiated primarily by a complex containing ULK1 or ULK2 (two ... ...

Abstract	Abstract Macroautophagy, the degradation of cytoplasmic content by lysosomal fusion, is an evolutionary conserved process promoting homeostasis and intracellular defence. Macroautophagy is initiated primarily by a complex containing ULK1 or ULK2 (two paralogs of the yeast Atg1 protein). To understand the differences between ULK1 and ULK2, we compared the human ULK1 and ULK2 proteins and their regulation. Despite the similarity in their enzymatic domain, we found that ULK1 and ULK2 have major differences in their autophagy-related interactors and their post-translational and transcriptional regulators. We identified 18 ULK1-specific and 7 ULK2-specific protein motifs serving as different interaction interfaces. We found that interactors of ULK1 and ULK2 all have different tissue-specific expressions partially contributing to diverse and ULK-specific interaction networks in various tissues. We identified three ULK1-specific and one ULK2-specific transcription factor binding sites, and eight sites shared by the regulatory region of both genes. Importantly, we found that both their post-translational and transcriptional regulators are involved in distinct biological processes—suggesting separate functions for ULK1 and ULK2. Unravelling differences between ULK1 and ULK2 could lead to a better understanding of how ULK-type specific dysregulation affects autophagy and other cellular processes that have been implicated in diseases such as inflammatory bowel disease and cancer.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2020-07-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Evolution of regulatory networks associated with traits under selection in cichlids

Tarang K. Mehta / Christopher Koch / Will Nash / Sara A. Knaack / Padhmanand Sudhakar / Marton Olbei / Sarah Bastkowski / Luca Penso-Dolfin / Tamas Korcsmaros / Wilfried Haerty / Sushmita Roy / Federica Di-Palma

Genome Biology, Vol 22, Iss 1, Pp 1-

2021 Volume 28

Abstract: Abstract Background Seminal studies of vertebrate protein evolution speculated that gene regulatory changes can drive anatomical innovations. However, very little is known about gene regulatory network (GRN) evolution associated with phenotypic effect ... ...

Abstract	Abstract Background Seminal studies of vertebrate protein evolution speculated that gene regulatory changes can drive anatomical innovations. However, very little is known about gene regulatory network (GRN) evolution associated with phenotypic effect across ecologically diverse species. Here we use a novel approach for comparative GRN analysis in vertebrate species to study GRN evolution in representative species of the most striking examples of adaptive radiations, the East African cichlids. We previously demonstrated how the explosive phenotypic diversification of East African cichlids can be attributed to diverse molecular mechanisms, including accelerated regulatory sequence evolution and gene expression divergence. Results To investigate these mechanisms across species at a genome-wide scale, we develop a novel computational pipeline that predicts regulators for co-extant and ancestral co-expression modules along a phylogeny, and candidate regulatory regions associated with traits under selection in cichlids. As a case study, we apply our approach to a well-studied adaptive trait—the visual system—for which we report striking cases of network rewiring for visual opsin genes, identify discrete regulatory variants, and investigate their association with cichlid visual system evolution. In regulatory regions of visual opsin genes, in vitro assays confirm that transcription factor binding site mutations disrupt regulatory edges across species and segregate according to lake species phylogeny and ecology, suggesting GRN rewiring in radiating cichlids. Conclusions Our approach reveals numerous novel potential candidate regulators and regulatory regions across cichlid genomes, including some novel and some previously reported associations to known adaptive evolutionary traits.
Keywords	Gene regulatory network ; Co-expression ; Cichlid ; Opsin ; Molecular evolution ; Biology (General) ; QH301-705.5 ; Genetics ; QH426-470
Subject code	570
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: CytokineLink

Marton Olbei / John P. Thomas / Isabelle Hautefort / Agatha Treveil / Balazs Bohar / Matthew Madgwick / Lejla Gul / Luca Csabai / Dezso Modos / Tamas Korcsmaros

Cells, Vol 10, Iss 2242, p

A Cytokine Communication Map to Analyse Immune Responses—Case Studies in Inflammatory Bowel Disease and COVID-19

2021 Volume 2242

Abstract: Intercellular communication mediated by cytokines is critical to the development of immune responses, particularly in the context of infectious and inflammatory diseases. By releasing these small molecular weight peptides, the source cells can influence ... ...

Abstract	Intercellular communication mediated by cytokines is critical to the development of immune responses, particularly in the context of infectious and inflammatory diseases. By releasing these small molecular weight peptides, the source cells can influence numerous intracellular processes in the target cells, including the secretion of other cytokines downstream. However, there are no readily available bioinformatic resources that can model cytokine–cytokine interactions. In this effort, we built a communication map between major tissues and blood cells that reveals how cytokine-mediated intercellular networks form during homeostatic conditions. We collated the most prevalent cytokines from the literature and assigned the proteins and their corresponding receptors to source tissue and blood cell types based on enriched consensus RNA-Seq data from the Human Protein Atlas database. To assign more confidence to the interactions, we integrated the literature information on cell–cytokine interactions from two systems of immunology databases, immuneXpresso and ImmunoGlobe. From the collated information, we defined two metanetworks: a cell–cell communication network connected by cytokines; and a cytokine–cytokine interaction network depicting the potential ways in which cytokines can affect the activity of each other. Using expression data from disease states, we then applied this resource to reveal perturbations in cytokine-mediated intercellular signalling in inflammatory and infectious diseases (ulcerative colitis and COVID-19, respectively). For ulcerative colitis, with CytokineLink, we demonstrated a significant rewiring of cytokine-mediated intercellular communication between non-inflamed and inflamed colonic tissues. For COVID-19, we were able to identify cell types and cytokine interactions following SARS-CoV-2 infection, highlighting important cytokine interactions that might contribute to severe illness in a subgroup of patients. Such findings have the potential to inform the development of novel, ...
Keywords	cytokine ; network ; resource ; Cytoscape ; NDEx ; COVID-19 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: ViralLink

Agatha Treveil / Balazs Bohar / Padhmanand Sudhakar / Lejla Gul / Luca Csabai / Marton Olbei / Martina Poletti / Matthew Madgwick / Tahila Andrighetti / Isabelle Hautefort / Dezso Modos / Tamas Korcsmaros

PLoS Computational Biology, Vol 17, Iss 2, p e

An integrated workflow to investigate the effect of SARS-CoV-2 on intracellular signalling and regulatory pathways.

2021 Volume 1008685

Abstract: The SARS-CoV-2 pandemic of 2020 has mobilised scientists around the globe to research all aspects of the coronavirus virus and its infection. For fruitful and rapid investigation of viral pathomechanisms, a collaborative and interdisciplinary approach is ...

Abstract	The SARS-CoV-2 pandemic of 2020 has mobilised scientists around the globe to research all aspects of the coronavirus virus and its infection. For fruitful and rapid investigation of viral pathomechanisms, a collaborative and interdisciplinary approach is required. Therefore, we have developed ViralLink: a systems biology workflow which reconstructs and analyses networks representing the effect of viruses on intracellular signalling. These networks trace the flow of signal from intracellular viral proteins through their human binding proteins and downstream signalling pathways, ending with transcription factors regulating genes differentially expressed upon viral exposure. In this way, the workflow provides a mechanistic insight from previously identified knowledge of virally infected cells. By default, the workflow is set up to analyse the intracellular effects of SARS-CoV-2, requiring only transcriptomics counts data as input from the user: thus, encouraging and enabling rapid multidisciplinary research. However, the wide-ranging applicability and modularity of the workflow facilitates customisation of viral context, a priori interactions and analysis methods. Through a case study of SARS-CoV-2 infected bronchial/tracheal epithelial cells, we evidence the functionality of the workflow and its ability to identify key pathways and proteins in the cellular response to infection. The application of ViralLink to different viral infections in a context specific manner using different available transcriptomics datasets will uncover key mechanisms in viral pathogenesis.
Keywords	Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Integrated intra‐ and intercellular signaling knowledge for multicellular omics analysis

Dénes Türei / Alberto Valdeolivas / Lejla Gul / Nicolàs Palacio‐Escat / Michal Klein / Olga Ivanova / Márton Ölbei / Attila Gábor / Fabian Theis / Dezső Módos / Tamás Korcsmáros / Julio Saez‐Rodriguez

Molecular Systems Biology, Vol 17, Iss 3, Pp n/a-n/a (2021)

2021

Abstract: Abstract Molecular knowledge of biological processes is a cornerstone in omics data analysis. Applied to single‐cell data, such analyses provide mechanistic insights into individual cells and their interactions. However, knowledge of intercellular ... ...

Abstract	Abstract Molecular knowledge of biological processes is a cornerstone in omics data analysis. Applied to single‐cell data, such analyses provide mechanistic insights into individual cells and their interactions. However, knowledge of intercellular communication is scarce, scattered across resources, and not linked to intracellular processes. To address this gap, we combined over 100 resources covering interactions and roles of proteins in inter‐ and intracellular signaling, as well as transcriptional and post‐transcriptional regulation. We added protein complex information and annotations on function, localization, and role in diseases for each protein. The resource is available for human, and via homology translation for mouse and rat. The data are accessible via OmniPath’s web service (https://omnipathdb.org/), a Cytoscape plug‐in, and packages in R/Bioconductor and Python, providing access options for computational and experimental scientists. We created workflows with tutorials to facilitate the analysis of cell–cell interactions and affected downstream intracellular signaling processes. OmniPath provides a single access point to knowledge spanning intra‐ and intercellular processes for data analysis, as we demonstrate in applications studying SARS‐CoV‐2 infection and ulcerative colitis.
Keywords	intercellular signaling ; ligand‐receptor interactions ; omics integration ; pathways ; signaling network ; Biology (General) ; QH301-705.5 ; Medicine (General) ; R5-920
Subject code	612
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Immune checkpoint inhibitor-induced colitis is mediated by polyfunctional lymphocytes and is dependent on an IL23/IFNγ axis

Jonathan W. Lo / Domenico Cozzetto / James L. Alexander / Nathan P. Danckert / Matthew Madgwick / Naomi Knox / Jillian Yong Xin Sieh / Marton Olbei / Zhigang Liu / Hajir Ibraheim / Jesus Miguens Blanco / Hiromi Kudo / Rocio Castro Seoane / Lucia A. Possamai / Robert Goldin / Julian Marchesi / Tamas Korcsmaros / Graham M. Lord / Nick Powell

Nature Communications, Vol 14, Iss 1, Pp 1-

2023 Volume 20

Abstract: Abstract Immune checkpoint inhibitors (CPIs) are a relatively newly licenced cancer treatment, which make a once previously untreatable disease now amenable to a potential cure. Combination regimens of anti-CTLA4 and anti-PD-1 show enhanced efficacy but ... ...

Abstract	Abstract Immune checkpoint inhibitors (CPIs) are a relatively newly licenced cancer treatment, which make a once previously untreatable disease now amenable to a potential cure. Combination regimens of anti-CTLA4 and anti-PD-1 show enhanced efficacy but are prone to off-target immune-mediated tissue injury, particularly at the barrier surfaces. To probe the impact of immune checkpoints on intestinal homoeostasis, mice are challenged with anti-CTLA4 and anti-PD-1 immunotherapy and manipulation of the intestinal microbiota. The immune profile of the colon of these mice with CPI-colitis is analysed using bulk RNA sequencing, single-cell RNA sequencing and flow cytometry. CPI-colitis in mice is dependent on the composition of the intestinal microbiota and by the induction of lymphocytes expressing interferon-γ (IFNγ), cytotoxicity molecules and other pro-inflammatory cytokines/chemokines. This pre-clinical model of CPI-colitis could be attenuated following blockade of the IL23/IFNγ axis. Therapeutic targeting of IFNγ-producing lymphocytes or regulatory networks, may hold the key to reversing CPI-colitis.
Keywords	Science ; Q
Subject code	570
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mapping the epithelial–immune cell interactome upon infection in the gut and the upper airways

Martina Poletti / Agatha Treveil / Luca Csabai / Leila Gul / Dezso Modos / Matthew Madgwick / Marton Olbei / Balazs Bohar / Alberto Valdeolivas / Denes Turei / Bram Verstockt / Sergio Triana / Theodore Alexandrov / Julio Saez-Rodriguez / Megan L. Stanifer / Steeve Boulant / Tamas Korcsmaros

npj Systems Biology and Applications, Vol 8, Iss 1, Pp 1-

2022 Volume 19

Abstract: Abstract Increasing evidence points towards the key role of the epithelium in the systemic and over-activated immune response to viral infection, including SARS-CoV-2 infection. Yet, how viral infection alters epithelial–immune cell interactions ... ...

Abstract	Abstract Increasing evidence points towards the key role of the epithelium in the systemic and over-activated immune response to viral infection, including SARS-CoV-2 infection. Yet, how viral infection alters epithelial–immune cell interactions regulating inflammatory responses, is not well known. Available experimental approaches are insufficient to properly analyse this complex system, and computational predictions and targeted data integration are needed as an alternative approach. In this work, we propose an integrated computational biology framework that models how infection alters intracellular signalling of epithelial cells and how this change impacts the systemic immune response through modified interactions between epithelial cells and local immune cell populations. As a proof-of-concept, we focused on the role of intestinal and upper-airway epithelial infection. To characterise the modified epithelial–immune interactome, we integrated intra- and intercellular networks with single-cell RNA-seq data from SARS-CoV-2 infected human ileal and colonic organoids as well as from infected airway ciliated epithelial cells. This integrated methodology has proven useful to point out specific epithelial–immune interactions driving inflammation during disease response, and propose relevant molecular targets to guide focused experimental analysis.
Keywords	Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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