Hub members Have many expertise, covering most of the fields in bioinformatics and biostatistics. You'll find below a non-exhaustive list of these expertise
Searched keyword : Epigenomics
Related people (4)
After a Master degree in Genetics at Magistère Européen de Génétique, Paris Diderot, I did a second Master in bioinformatics at University of Nantes where I focused my work on the study of mapping strategy for allele specific analysis at the bioinformatics platform of Institut Curie. I then joined Institut Pasteur to work on an ELIXIR project related to the bio.tools registry through the development of a dedicated tool and the participation of several workshops and hackathons. As an engineer of the bioinformatics and Biostatistics Hub, I am involved in several projects from Differential Analysis of RNA-seq data to Metagenomics. I am also in charge of the maintenance of the Galaxy Pasteur instance.
ChIP-seqEpigenomicsGenomicsSequence analysisProgram developmentDatabases and ontologiesSofware development and engineeringGeneticsData integrationRead mappingWorkflow and pipeline developmentConfocal Microscopy
- Impact of gut microbiota on lipid metabolism(Grégoire CHEVALIER - Microenvironment and Immunity) - Closed
- Analysis of IFITM RNA levels in vraious cell types and tissues(Olivier SCHWARTZ - Virus and Immunity) - Closed
- Channels in metagenomics data(Delarue MARC - Structural Dynamics of Macromolecules) - Closed + 1 project
Rachel Legendre is a bioinformatics engineer. She completed her master degree in apprenticeship for two years at INRA in Jouy-en-Josas in the Genetic Animal department. She was involved in a project aiming at the detection and the expression analysis of micro-RNA involved in an equine disease. In 2012, she joined the Genomic, Structure and Translation Team at Paris-Sud (Paris XI) university. She worked principally on Ribosome Profiling data analysis, a new technique that allows to identify the position of the ribosome on the mRNA at the nucleotide level. Since november 2015, she worked at Institut Pasteur. During 4 years, she was detached to the Biomics Platform, where she was in charge of the bioinformatics analyses for transcriptomics and epigenomics projects. She was also involved in Long Reads (PacBio and Nanopore) developments with other bioinformaticians of Biomics. Since november 2019, she has joined the Hub of Bioinformatics and Biostatistics, et more precisely the Genome Organization Regulation and Expression group.
AlgorithmicsChIP-seqEpigenomicsNon coding RNATranscriptomicsGenome analysisProgram developmentScientific computingSofware development and engineeringIllumina HiSeqRead mappingSequencingWorkflow and pipeline developmentChromatin accessibility assaysPac BioRibosome profiling
BacteriaFungiParasiteHumanInsect or arthropodOther animal
- CHIP-seq identification of IRF8 binding site(Ludivine GRZELAK - Virus and Immunity) - Awaiting Publication
- Exploring pathogenic mechanisms of chronic inflammatory disease: unresolved issues in IL-23/IL-17 biology(YAHIA HANANE - Immunoregulation) - In Progress
- Identification of factors influencing the activity of bacteriophage within the gut of mammals(Devon CONTI - Other) - In Progress
After graduating from Paris VI University with a PhD in Genetics on the “Role of histone protein post-translational modifications in splicing regulation” that I performed in the Epigenetic Regulation unit at the Institut Pasteur, I carried out two post-doctoral experiences. I first worked for three years as a postdoctoral associate of the Whitehead Institute for Biomedical Research/MIT in Cambridge (USA). My main project consisted in the integration of genomic and epigenomic data in order to predict the transcription factors that are potentially at the core of the regulation of the cell-type specific gene expression programs. I then joined the Institut Curie where I deepened my experience in multi-omics data analyses and integration to identify non-coding RNAs involved in cancer progression. I have recently joined the HUB-C3BI of the Institut Pasteur where I am performing high-throughput data integration to better understand biological complexity and contribute to precision medicine development.
ATAC-seqChIP-seqEpigenomicsNon coding RNAPathway AnalysisRNA-seqSingle CellSystems BiologyTool DevelopmentTranscriptomicsData integrationGraph theory and analysisCell biology and developmental biology
Related projects (8)
The post-translational modification by SUMO is an essential regulatory mechanism of protein function that is involved in most challenges faced by eukaryotic cells. Gene expression is particularly regulated by sumoylation as many SUMO substrates are transcription factors and chromatin-associated proteins, including histones. The emerging paradigm for the proposed work is that sumoylation controls multiple aspects of chromatin structure and function in response to external cues. According to this view, sumoylation is expected to impact both global and specific transcriptional programs thereby affecting constitutive and inducible expression of both coding and non coding genes. Recently, we found SUMO as an integral and instructive component of chromatin in cell growth and senescence, thus establishing sumoylation as a new and paradigmatic chromatin modification. This work now paves the way for detailed understanding of the contribution of SUMO as a multifaceted modifier of chromatin.
Methylome analysis of a human progeroid disease for the detection of progeroid-specific alterations and their link with regular ageing
The mechanisms governing ageing, which is a multifactorial process, have not been resolved and constitute a fundamental open question in cell and organismal biology. Exceptionally, in rare genetic diseases like the Cockayne syndrome (CS), ageing is dramatically accelerated. We have recently identified a novel pathway that is altered in cells from CS patients and is not affected in a linked disease (UVSS) that is not associated with precocious ageing. This is a unique case in the literature of diseases due to mutations in the same proteins but only one resulting in precocious ageing. The defect linked to the progeroid phenotype consists in oxidative stress-dependent overexpression of a little known proteases, HTRA3, which degrades the key mitochondrial DNA polymerase and in turn affects mitochondrial function. We succeeded in rescuing the defective phenotype in patient cells using two independent strategies. We aim to understand the mechanism by which oxidative stress induces overexpression of HTRA3 and we have indications that this event may be linked to the methylation of target genes. Genome wide methylation will be analysed in these rare patient cells.
Analysis of DNA methylation in the presence and absence of antibiotics in wt and mutant V. cholerae.
Thanks to RNA-Seq experiments we identified a new orphan DNA methylase (not associated with a restriction enzyme) that is highly upregulated in the presence of low concentrations of aminoglycosides in V. cholerae. The results allow us to consider a differential DNA methylation profile depending on the environment (with or without antibiotics), which can possibly correspond to a novel epigenetic control of the response.
Enhancers of transcription are regulatory sequences enabling gene expression from a distance. The landscape of active enhancers is cell-type specific and provides extensive information on the transcription factors at play. Currently, enhancers are mostly mapped based on the histone modifications positioned on their DNA sequence. This type of data is abundantly available for tumor-derived tissue culture cells, but difficult to obtain when the biological material has a limited availability. As an alternative approach, it is possible to detect enhancers as sites of divergent transcription. The objective of this project will be to develop tools allowing detection of sites of divergent transcription in transcriptome and run-on data, to evaluate the quality of the prediction by comparing the outcome with existing enhancer maps, and then ultimately use this approach to identify changes in the enhancer landscape between patients with multiple sclerosis and healthy controls.
Characterization of the role of Argonaute proteins in regulating germline gene expression at the transcriptional and the post-transcriptional levels.
This research project focuses on the characterization of the role of small RNAs and their associated Argonaute proteins in transcriptional and post-transcriptional regulation of germline gene expression. Using the nematode C. elegans, we have recently showed that one of the germline-expressed Argonaute protein, CSR-1, promotes germline transcription. However, CSR-1 also possess an endonucleolytic activity that might participate in post-transcriptional silencing. Therefore, two possible functions of the protein might regulate the germline transcriptome. 1) CSR-1 promotes specific germline transcription programs in the nucleus, and 2) negatively regulates expression of target transcripts in the cytoplasm. To gain mechanistic insights into these two functions, we aim to use RNA-seq, sRNA-seq, ChIP-seq, GRO-seq, Ribo-seq, RIP-seq, iCLIP in wild type worms, knock out and catalytic inactive mutants of CSR-1 protein at different times of germline development.
It has been shown that methylation can act as a kind of memory of the immune system. For patients with co-infections, it is of particular importance to know when to begin an anti-retroviral therapy, especially if they are already infected with tuberculosis. The goal of this study is to find hyper or hypo methylated loci related to the reaction of HIV patients (co-infected or not) to different kind of treatments.
Cellular senescence is a complex stress response that durable (yet not irreversibly) arrests cell proliferation and is accompanied by widespread changes in chromatin structure, metabolism and gene expression including the production and secretion of a plethora of inflammatory factors. Cellular senescence plays beneficial roles during embryonic development, tissue regeneration, and tumor suppression. Paradoxically, it is also considered a major contributor to aging and age-related diseases, the latter mostly through its inflammatory phenotype, the so-called SASP (senescence-associated secretory phenotype). The proposed work aims at integrating time-resolved transcriptome, ChIP-seq, and ATAC-seq datasets into a comprehensive understanding of senescence-associated gene regulation.
We are in the process of publishing a paper showing that IRF8, a transcription factor, regulates MS4A1 expression. Indeed, we showed IRF8 was necessary for MS4A1 expression by knocking-out the gene. A reviewer is asking us to directly assess IRF8 binding on MS4A1 gene using already published CHIP-seq data (PMID:31000603).