Best Poster Awards – Target Validation Using Genomics and Informatics

Meet Giovanni Spirito and Borja Gomez Ramos – the two poster prize winners at the recent EMBL – Wellcome Genome Campus Conference: Target Validation Using Genomics and Informatics (8 – 10 Dec 2019).

Identification and prioritization of candidate causal genomic variations from individuals affected by ASD

PHOTO: Giovanni Spirito

Authors: Giovanni Spirito (1), Diego Vozzi (2), Martina Servetti (3), Margherita Lerone (3), Maria Teresa Divizia (3), Giulia Rosti (3), Livia Pisciotta (4), Lino Nobili (4), Irene Serio (4), Stefano Gustincich (2), Remo Sanges (1)

Next generation sequencing (NGS) technologies enabled the extensive study of the genomics underlying human diseases. Namely whole exome sequencing (WES) represents a cost-efficient method which can lead to the detection of multiple classes of genomic variants and the discovery of novel disease-associated genes. One of the drawbacks of this approach however, is the large number of genomic variants detected in each analysis. Automated variant prioritization strategies are therefore required. This is particularly important in the case of complex disease such as ASD, whose genetic etiology is still poorly understood. To this aim we built a custom computational framework capable, from raw WES data, to automatically detect four classes of genomic variants (SNPs, indels, copy number variants and short tandem repeat variants) and prioritize them in regards to their relevance to a specific phenotype. We tested this framework on a selection of 29 trios including probands affected by severe and undiagnosed rare phenotypes and a small cohort of 10 trios all featuring healthy parents and one offspring affected by autism spectrum disorder (ASD). We were able to successfully detect rare and de novo high penetrance variants which have been validated and confirmed as causative among the undiagnosed probands. In the specific case of the ASD cohort we could highlight several genes which are not implicated in autism susceptibility, but nevertheless whose connections to genes relevant for ASD could suggest a possible involvement in the phenotype. Furthermore, our approach enabled us to detect several instances characterized by the presence of multiple candidate variants within genes belonging to the same canonical pathway in one proband. Our workflow allows to detect and prioritize multiple classes of genomic variants in order to both highlight rare high penetrance disease-causative mutation, and possibly reconstruct the genomics at the basis of complex ASD phenotypes.

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(1) SISSA, Italy, (2) IIT, Italy, (3) Gaslini Institute, Italy, (4) University of Genova, Italy


Omics data integration for the identification of cell-type-specific gene regulatory networks and regulatory variants in Parkinson’s disease

PHOTO: Borja Gomez Ramos

Authors: Borja Gomez Ramos (1,2), Jochen Ohnmacht (1,2), Nikola de Lange (2), Aurélien Ginolhac (1), Aleksandar Rakovic (5), Christine Klein (5), Roland Krause (2) , Marcel H. Schulz (6), Thomas Sauter (1), Rejko Krüger (2,3,4) and Lasse Sinkkonen (1)

Genome-Wide Association Studies (GWAS) have identified many variants associated with different diseases. However, it is still a challenge to make sense of this data as the majority of genetic variants are located in non-coding regions, complicating the understanding of their functionality. In the last few years, it has been found that non-coding genetic variants concentrate in regulatory regions in the genome, which are cell type and cell-stage specific. In this project, we seek to identify functional Parkinson’s disease GWAS non-coding genetic variants that could make carriers more prone to developing PD. To do so, we are using induced pluripotent stem cell (iPSC) technology to differentiate somatic cells into midbrain dopaminergic (mDA) neurons, astrocytes and microglia. Assessing their chromatin accessibility, active chromatin regions and transcriptome, we can identify crucial regulatory regions in the genome, key transcription factors and derive the gene regulatory networks for the three different cell types. Then, we will map the non-coding genetic variants to the different regulatory regions and predict their effect in silico for the subsequent validation in vitro. This innovative approach will also identify novel factors controlling cell fate and cell identity.

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(1) Life Sciences Research Unit, University of Luxembourg, Luxembourg, (2) Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg, Luxembourg, (3) Centre Hospitalier de Luxembourg (CHL), Luxembourg, (4) Luxembourg Institute of Health (LIH), Luxembourg, (5) Institute of Neurogenetics, University of Lübeck, Germany, (6) Institute for Cardiovascular Regeneration, Uniklinikum and Goethe University Frankfurt, Germany


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Best Poster Awards – Metabolism Meets Epigenetics

In its first edition, the EMBO|EMBL Symposium: Metabolism Meets Epigenetics brought together 289 world-leading researchers who examined how metabolites and metabolic networks impact gene regulation, what their roles are in disease and how this opens novel therapeutic avenues.

In addition to the 21 invited speakers and 22 selected short talks, 142 posters were presented during the two poster sessions. Today we present three of the five award-winning posters decided by popular vote.

Citrate carrier links intermediate metabolism to histone acetylation upon ageing of mouse mesenchymal stem cells (MSCs)

PHOTO: Andromachi Pouikli

Authors: Andromachi Pouikli (1), Monika Maleszewska (2), Swati Parekh (1), Chrysa Nikopoulou (1), Maarouf Baghdadi (1), Linda Partridge (1), Peter Tessarz (1)

Chromatin and metabolism interact in a reciprocal manner; on one hand metabolism-related genes are subjected to epigenetic modifications, which regulate gene expression. On the other hand, intracellular metabolism provides metabolites which can serve as essential co-factors and substrates for chromatin-modifying enzymes, affecting their activity. Although, it is well established that the process of ageing is accompanied by changes in metabolism and by chromatin alterations, their interplay in this context remains still poorly understood. In this study we sought to determine how ageing impinges on the relationship between cellular metabolism and the epigenome, using mouse mesenchymal stem cells from the bone marrow (BM-MSCs). In brief, our data suggest that there is a strong and direct link between the metabolic and the epigenetic states of the cell, with ageing-driven changes in metabolism regulating gene transcription and BM-MSC’s stemness, via alterations of the chromatin structure. We conclude that physiological ageing elicits changes in metabolism, resulting in suppressed glycolysis and impaired lipid biogenesis. Moreover, we demonstrate that during ageing there are lower levels of histone acetylation, despite the higher acetyl-CoA levels. We provide a solid explanation for this apparent discrepancy, pointing to the impaired export of acetyl-CoA from mitochondria to the cytosol. Indeed, the protein levels of the citrate carrier Slc25a1 decrease dramatically upon ageing. Using inhibition and supplementation experiments we provide a causal relationship between Slc25a1 function and the levels of histone acetylation, which directly influence chromatin accessibility and plasticity. Collectively, our data establish a tight, age-dependent connection between metabolism, epigenome and stemness and identify citrate carrier as the responsible protein for the mitochondrial-nuclear communication.

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(1) Max Planck Institute for Biology of Ageing, Germany, (2) Personalis Inc, Germany


Epigenetics meets metabolism through histone acetyltransferase NAA40

PHOTO: Christina Demetriadou

Authors: Christina Demetriadou (1), Anastasia Raoukka (1), Agathi Elpidoforou  (1), Constantine Mylonas (2), Swati Parekh (2), Peter Tessarz (2), Antonis Kirmizis (1)

N-alpha-acetyltransferase 40 (NAA40) is distinct among other histone acetyltransferases (HATs) because it deposits an acetyl moiety on the alpha-amino group at the very N-terminal tip of histones H4 and H2A, instead on the lysine side chain. The biological function of this evolutionarily conserved enzyme remained unexplored for several decades because it was thought to mediate an inert modification. However, we previously showed that NAA40-mediated N-terminal acetylation of histone H4 (N-acH4) crosstalks with an adjacent arginine methylation mark to regulate yeast cellular aging in response to caloric restriction through transcriptional control of several metabolic genes. Therefore, we are currently interested in deciphering the function of human NAA40 in carcinogenesis. We recently showed that NAA40 is frequently upregulated in primary human colorectal cancer (CRC) samples. Remarkably, depletion of NAA40 and its accompanied reduction in N-acH4 blocked colon cancer cell proliferation and reduced cell survival in vitro and in xenograft models. We also found that loss of NAA40 expression or of its HAT activity markedly induce global histone methylation. Additionally, whole transcriptome analysis showed that NAA40 knockdown leads to upregulation of key enzymes involved in one-carbon metabolism. Intriguingly, silencing of methylenetetrahydrofolate reductase (MTHFR), which links the folate to methionine cycle, rescues the induction of global histone methylation and loss of cell viability triggered by NAA40 depletion. Hence, this recent work implies that NAA40 may transcriptionally regulate vital metabolic enzymes to control the flux of carbon units into the methionine cycle influencing S-adenosylmethionine (SAM) levels and triggering epigenome reprogramming of cancer cells. Overall, our findings thus far propose that NAA40 and its associated N-acH4 are crucial epigenetic modulators in tumourigenesis and implicate these factors in rewiring cancer cell metabolism.

Poster currently not available.

(1) University of Cyprus, Cyprus
(2) Max Planck Institute for Biology of Ageing, Germany


Role of MOF acetyl transferase in mitochondrial homeostasis

PHOTO: Sukanya Guhathakurta

Authors: Sukanya Guhathakurta (1), Christoph Martensson (2), Alexander Schendzielorz (3), Bettina Warsheid (3), Thomas Becker (2), Asifa Akhtar (1)

Mitochondria lies at the centre of cellular and organismal energy homeostasis, housing a large repertoire of enzymes that are required for the synergy of various metabolic pathways. Mitochondrial gene expression and protein acetylation are two important fundamental processes situated at the crossroad between mitochondrial function and metabolic status of a cell. Gene transcription in the mitochondria has been studied over several decades, but enzymatic acetylation of mitochondria proteins has stayed so far enigmatic. MOF acetyl transferase and its KANSL complex members dually localize to the nucleus and the mitochondria in mouse and human cells. The MOF-KANSL complex regulates metabolic gene transcription in the nucleus and expression of Electron Transport Chain (mtETC) components from the mtDNA, in a cell type dependent fashion. Regulation of nuclear gene transcription by MOF is well understood, however, its control of mitochondrial function remains elusive. Here, we report that loss of MOF leads to severe mitochondrial dysfunction in Mouse Embryonic Fibroblasts (MEFs), sprouting from a stalled oxidative phosphorylation. We address the mechanisms by which the enzyme maintains mitochondrial function in these cells by using a multi-omics approach. We discovered that the role of MOF-KANSL complex in the mitochondria of aerobically respiring cells could be decoupled from its regulation of steady state RNA levels, and could further be attributed to the acetylation of mitochondrial proteins. We characterize the role of acetylation on these proteins through generation of acetylated and non-acetylated mimics. Collectively our data, along with previously published works, suggests that MOF has emerged as a moderator to strike a harmony in the context of communication between the nucleus and the mitochondria. Recent progress on the project will be discussed.

(1) Max Planck Institute for Immunobiology and Epigenetics, Germany
(2) Institute of Biochemistry and Molecular Biology, Germany
(3) Institute for Biology II, Germany

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Best Poster Awards – Precision Health

140 researchers came together recently at the EMBL Advanced Training Centre in Heidelberg, Germany, for the EMBO Workshop: Precision Health: Molecular Basis, Technology and Digital Health (13 – 16 November 2019) to present and discuss the promises and challenges of precision health and the molecular insights necessary to enable a maintenance of wellness and prevention of disease.

Out of the posters presented, 4 were awarded a poster prize based on popular vote. Here we present the poster abstracts of four of the winners.

A computational modelling approach to characterizing postprandial glucose responses in individuals
Balazs Erdos from TiFN Wageningen and MaCSBio, Maastricht University, The Netherlands, PHOTO: Balazs Erdos

Balazs Erdos (1), (2)*, Bart van Sloun (1), (2), Shauna O’Donovan (2), Michiel Adriaens (2), Natal van Riel (3), Ellen Blaak (4), Ilja Arts (2)

The large variability in the dynamic properties of the postprandial glucose response curves in individuals suggest that it is not sufficient to use average values or single time point measures of postprandial glycemia in order to characterize individuals’ glycemic control. Instead, approaches that are capable of capturing the dynamic events are necessary. In this study, we develop personalized computational models based on ordinary differential equations, to describe the glucose and insulin dynamics of individuals in response to an oral glucose tolerance test. We observed that these personalized models are capable of capturing a wide range of glucose and insulin dynamics including normal, prediabetic and type 2 diabetic responses as well as responses from intermediate states.

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(1) TiFN, Wageningen, The Netherlands, (2) Maastricht Centre for Systems Biology (MaCSBio), Maastricht University, Maastricht, The Netherlands, (3) Dept. of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands, (4) Dept. of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands

*E-mail: balazs.erdos@maastrichtuniversity.nl


Predict nephrotoxicity associated with cisplatin-based chemotherapy in testicular cancer patients

Sara Garcia (1), Jakob Lauritsen (2), Zeyu Zhang (3), Mikkel Bandak (2), Marlene Danner Dalgaard (1), Rikke Linnemann Nielsen (1), Gedske Daugaard (2), Ramneek Gupta (1)

In industrialized countries, testicular cancer (TC) is the most common solid tumor in men between 20 and 40 years old and besides being one of the most treatable types of cancer, the long-term side-effects of chemotherapy are worrisome, since they are largely irreversible. Their severity is normally related to the total amount of chemotherapy received, which makes that an important factor to a successful treatment. The standard treatment for TC is 3 cycles of cisplatin, etoposide and bleomycin (BEP), being that the number of cycles can vary between 4-5 or more if the prognosis of the patient is intermediate or poor. Some of the late side-effects include nephrotoxicity, which can be measured by the drop in glomerular filtration rate after the patient follows chemotherapy. Materials and Methods: Integrative machine learning models were built using a dataset of 400 Danish individuals in order to identify clinical and/or genomics features and classify patients at higher risk of developing nephrotoxicity given a treatment of BEP-cycles. Results: First, only clinical features, such as age at the time of treatment, dose of cisplatin, patient’s prognosis, and number of cycles, were considered, and relevant features were selected to use in the classifier (AUC 0.66, SD 0.02). The classifier was then optimized by adding genomics markers, which helped improving the prediction (AUC 0.75, SD 0.02). Conclusions: Therefore, it is proposed a machine learning algorithm which, by helping predicting nephrotoxicity in advance, can benefit to improve chemotherapy efficacy in TC patients. These data driven models can also be applicable to other cancers, such as ovarian, bladder, and lung cancer where more elderly patients are at risk of nephrotoxicity and identification upfront will have direct clinical implications.

Poster currently not available

(1) Technical University of Denmark, Denmark, (2) Copenhagen University Hospital, Denmark, (3) University of Chinese Academy of Sciences, China


Loss of N-glycanase 1 alters transcriptional and translational regulation
Petra Jakob from EMBL Heidelberg, Germany, PHOTO: Petra Jakob

Petra Jakob (1), William Mueller (1), Sandra Clauder-Münster (1), Han Sun (2), Sonja Ghidelli-Disse (3), Diana Ordonez (1), Markus Boesche (3), Markus Bantscheff (3), Paul Collier (1), Bettina Haase (1), Vladimir Benes (1), Malte Paulsen (1), Peter Sehr (1), Joe Lewis (1), Gerard Drewes (3), Lars Steinmetz (1)

N-Glycanase 1 (NGLY1) deficiency is an ultra-rare, complex and devastating neuromuscular disease. Patients display multi-organ symptoms including developmental delays, movement disorders, seizures, constipation and lack of tear production. NGLY1 is a deglycosylating protein involved in the degradation of misfolded proteins retrotranslocated from the endoplasmic reticulum (ER). NGLY1-deficient cells have been reported to exhibit decreased deglycosylation activity and an increased sensitivity to proteasome inhibitors. We show that the loss of NGLY1 causes substantial changes in the RNA and protein landscape of K562 cells and results in downregulation of proteasomal subunits, consistent with its processing of the transcription factor NFE2L1. We employed the CMap database to predict compounds that can modulate NGLY1 activity. Utilizing our robust K562 screening system, we demonstrate that the compound NVP-BEZ235 (Dactosilib) promotes degradation of NGLY1-dependent substrates, concurrent with increased autophagic flux, suggesting that stimulating autophagy may assist in clearing aberrant substrates during NGLY1 deficiency.

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(1) EMBL Heidelberg, Germany, (2) Stanford University, United States of America, (3) Cellzome, Germany


Data integration for prediction of weight loss in clinically controlled dietary trials

Rikke Linnemann Nielsen (1), Marianne Helenius (1), Sara Garcia (1), Henrik Munch Roager (2), Derya Aytan (3), Lea Benedicte Skov Hansen (1), Mads Vendelbo Lind (2), Josef Vogt (1), Marlene Danner Dalgaard (1), Martin I Bahl (3), Cecilia Bang Jensen (1), Rasa Muktupavela (1), Christina Warinner (4), Vincent Appel (5), Rikke Gøbel (5), Mette B Kristensen (2), Hanne Frøkjær (6), Morten H Sparholt (7), Anders F Christensen (7), Henrik Vestergaard (5), Torben Hansen (5), Karsten Kristiansen (6), Susanne Brix Pedersen (1), Thomas Nordahl Petersen (3), Lotte Lauritzen (2), Tine Rask Licht (3), Oluf Pedersen (5), Ramneek Gupta (1)

Diet is a key strategy in weight loss management. Advances in omics technologies research allow analyses of determinants of clinical interventions outcomes. We have previously reported diet-induced weight loss in non-diabetic middle-aged Danes in two clinically controlled dietary trials where the content of whole grain or gluten was changed. However, it remains elusive how predictable weight loss is at the individual level. We here classify weight loss responders and non-responders from the whole grain and gluten trials by integrating multi-omics data (host genetics, gut microbiome, urine metabolome) together with physiology and anthropometrics into random forest models. The most predictive models for weight loss included features of diet, gut microbial species and urine metabolites (ROC-AUC:0.84-0.88, model only with diet type ROC-AUC:0.62). Furthermore, we demonstrate that a model ensemble is robust to missing information of microbiome and metabolome profiles given features of physiology (including postprandial response), host genetics and transit-time (ROC-AUC:0.72).

Poster currently not available

(1) Technical University of Denmark, Denmark, (2) University of Copenhagen, National Food Institute, Technical University of Denmark, Denmark, (3) National Food Institute, Technical University of Denmark, Denmark, (4) Harvard University, United States of America, (5) The Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Denmark, (6) University of Copenhagen, Denmark, (7) Bispebjerg University Hospital, Denmark


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Best Poster Awards – Cancer Genomics

The 4th EMBL Conference: Cancer Genomics (4 – 6 November 2019) brought together over 240 scientists in the field of cancer research to present the latest findings in cancer functional genomics, systems biology, cancer immunogenomics and epigenomics, as well as their translation and clinical impact.

123 posters were presented at the two poster sessions, out of which two were selected as the winners by popular vote. 

Infinite sites violations during tumour evolution reveal local mutational determinants

Jonas Demeulemeester is a postdoctoral researcher at the Francis Crick Insitute in UK. PHOTO: Jonas Demeulemeester

Authors: Jonas Demeulemeester (1), Stefan C. Dentro (2), Moritz Gerstung (2), Peter Van Loo (1)

The infinite sites model of molecular evolution requires that every base in the genome is mutated at most once. It is a cornerstone of (tumour) phylogenetic analysis, and is often implied when calling, phasing and interpreting variants or studying the mutational landscape as a whole. It is unclear however, whether this assumption holds in practice for bulk tumour samples. Here we provide frameworks to model and detect infinite sites violations, identifying 24,459 in total, including 6 candidate biallelic driver events, in 700 bulk tumour samples (26.3%) from the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes project. Violations generally occur at mutational hotspots and their frequency and type can accurately be predicted from the overall mutation spectrum. In melanoma, their local sequence context evidences how not only ETS, but also NFAT-family transcription factor binding creates hotspots for UV-induced cyclobutane pyrimidine dimer formation. In colorectal adenocarcinoma, violations reveal hypermutable special cases of the trinucleotide mutational contexts identified in POLE-mutant tumours. Taken together, we reveal the infinite sites model breaks down at the bulk level for a considerable fraction of tumours. These results warrant a careful evaluation of current pipelines relying on the validity of the infinite sites assumption, especially when scaling up to larger sets of mutations and lineages in the future.

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(1) The Francis Crick Institute, United Kingdom, (2) EMBL-EBI, United Kingdom


The other award-winning poster was:

Understanding the early impact of activating PIK3CA mutation on cellular and genetic heterogeneity presented by Evelyn Lau, UCL Cancer Institute, United Kingdom


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Best Poster Awards – The Non-Coding Genome

Taking place for the third time,  the EMBO|EMBL Symposium: The Non-Coding Genome (16 – 19 October 2019) brought together 305 RNA experts to discuss the roles of non-coding RNAs in both prokaryotes and eukaryotes, gene regulation and function. 

A total of 189 posters were presented, from which two were singled out as the winners by popular vote.

Characterization of the genomic and splicing features of long non-coding RNAs using bioinformatics approaches

Monah Abou Alezz is a Ph.D student in genetics, molecular and cellular biology at the University of Pavia, Italy. PHOTO: Monah Abou Alezz

Authors: Monah Abou Alezz, Ludovica Celli, Giulia Belotti, Silvia Bione, Institute of Molecular Genetics L. L Cavalli-Sforza – National Research Council, Italy

Recent developments in deep sequencing approaches have simulated the continuous discovery of a significantly large number of novel long non-coding RNA (lncRNA) genes loci in the genomes. Long non-coding RNAs are recognized as a new class of regulatory molecules despite very little is known about their functions in the cellular processes. Due to their overall low expression level and tissue-specificity, the identification and annotation of lncRNA genes still remains challenging. The characterization of lncRNAs’ features is crucial to understand and get functional insights on their mechanisms of action. We exploited recent annotations by the GENCODE compendium to characterize the genomic and splicing features of long non-coding genes, in comparison to protein-coding ones, in the human and mouse genome by using bioinformatics approaches. Our analysis highlighted differences between the two classes of genes in terms of gene architecture regarding exons and introns length, GC-content, and the combinatorial patterns of chromatin marks and states. Moreover, significant differences in the splice sites usage were observed between long non-coding and protein-coding genes. While the frequency of non-canonical GC-AG splice junctions represents about 0.8% of total splice sites in protein-coding genes, we identified a remarkable enrichment of the GC-AG splice sites in long non-coding genes, both in human (3.0%) and mouse (1.9%). In addition, we identified peculiar characteristics of the GC-AG introns in terms of donor and acceptor splice sites strength, poly-pyrimidine tract, intron length, and a positional bias of GC-AG junctions being enriched in the first intron. Genes containing at least one GC-AG intron were found conserved in many species across large evolutionary distances, more prone to alternative splicing and a functional analysis pointed toward their enrichment in specific biological processes such as
DNA repair.

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MirGeneDB 2.0: The metazoan microRNA complement

Bastian Fromm is a Senior Researcher at Science for Life Laboratory, Stockholm University, Sweden. PHOTO: Bastian Fromm

Authors: Bastian Fromm (1), Diana Domanska (2), Eirik Hoye (3), Vladimir Ovchinnikov (4), Wenjing Kang (5), Ernesto Aparicio-Puerta (6), Morten Johansen (7), Kjersti Flatmark (3), Anthony Mathelier (8), Hovig
Eivind (3), Michael Hackenberg (6), Marc Friedländer (5), Kevin Peterson (9)

Non-coding RNAs (ncRNA) have gained substantial attention due to their roles in human disorders and animal development. microRNAs (miRNAs) are unique within this class as they are the only ncRNAs with individual gene sequences conserved across the animal kingdom. Bona fide miRNAs can be clearly distinguished from the myriad small RNAs generated in cells by a set of unique criteria. Unfortunately, recognition and utilization of these clear and mechanistically well understood features is not a  common practice. We addressed this by extensively expanding our curated miRNA gene database MirGeneDB to 45 organisms that represent the breadth of Metazoa. By consistently annotating and naming more than 11,000 miRNA genes in these organisms, we show that previous miRNA annotations contained not only many false positives, but surprisingly many false negatives as well. Indeed, curated miRNA complements of closely related organisms are very similar and can be used to reconstruct evolution of miRNA genes, families and biogenesis across more than 1 billion years of evolution. MirGeneDB represents a robust platform for providing deeper and more significant insights into the biology of miRNAs, possible sources of mis-regulation, and evolutionary mechanisms. MirGeneDB is publicly and freely available under http://mirgenedb.org/.

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Fromm, B. et al. MirGeneDB 2.0: the metazoan microRNA complement. Nucleic Acids Research, gkz885, (2019), https://doi.org/10.1093/nar/gkz885

(1) Science for Life Laboratory, Sweden
(2) Department of Informatics, University of Oslo, Oslo, Norway
(3) Department of Tumor Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
(4) School of Life Sciences, Faculty of Health and Life Sciences, University of Nottingham, United Kingdom
(5) Stockholm University, SciLifeLab, Sweden
(6) Department of Genetics, Faculty of Sciences, University of Granada, Granada, Spain
(7) Institute for Medical Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
(8) Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo, Oslo, Norway
(9) Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire, United States of America


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