Selected Publications

Better protocols and decreasing costs have made high-throughput sequencing experiments now accessible even to small experimental laboratories. However, comparing one or few experiments generated by an individual lab to the vast amount of relevant data freely available in the public domain might be limited due to lack of bioinformatics expertise. Though several tools, including genome browsers, allow such comparison at a single gene level, they do not provide a genome-wide view. We developed Heat*seq, a web-tool that allows genome scale comparison of high throughput experiments chromatin immuno-precipitation followed by sequencing, RNA-sequencing and Cap Analysis of Gene Expression) provided by a user, to the data in the public domain. Heat*seq currently contains over 12 000 experiments across diverse tissues and cell types in human, mouse and drosophila. Heat*seq displays interactive correlation heatmaps, with an ability to dynamically subset datasets to contextualize user experiments. High quality figures and tables are produced and can be downloaded in multiple formats. AVAILABILITY AND IMPLEMENTATION: Web application: http://www.heatstarseq.roslin.ed.ac.uk/ Source code: https://github.com/gdevailly
In: Bioinformatics (Oxford, England), (32), 21, pp. 3354–3356, https://doi.org/10.1093/bioinformatics/btw407, 2016

DNA methylation is thought to induce transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators unable to bind their target sites when methylated, and the recruitment of transcriptional repressors with specific affinity for methylated DNA. The Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. Here, we present MBD2 ChIPseq data obtained from the endogenous MBD2 in an isogenic cellular model of oncogenic transformation of human mammary cells. In immortalized (HMEC-hTERT) or transformed (HMLER) cells, MBD2 was found in a large proportion of methylated regions and associated with transcriptional silencing. A redistribution of MBD2 on methylated DNA occurred during oncogenic transformation, frequently independently of local DNA methylation changes. Genes downregulated during HMEC-hTERT transformation preferentially gained MBD2 on their promoter. Furthermore, depletion of MBD2 induced an upregulation of MBD2-bound genes methylated at their promoter regions, in HMLER cells. Among the 3,160 genes downregulated in transformed cells, 380 genes were methylated at their promoter regions in both cell lines, specifically associated by MBD2 in HMLER cells, and upregulated upon MBD2 depletion in HMLER. The transcriptional MBD2-dependent downregulation occurring during oncogenic transformation was also observed in two additional models of mammary cell transformation. Thus, the dynamics of MBD2 deposition across methylated DNA regions was associated with the oncogenic transformation of human mammary cells.
In: Nucleic Acids Research, (43), 12, pp. 5838–5854, https://doi.org/10.1093/nar/gkv508, 2015

Recent Publications

More Publications

. Causal Transcription Regulatory Network Inference Using Enhancer Activity as a Causal Anchor. In: International Journal of Molecular Sciences, (19), 11, https://doi.org/10.3390/ijms19113609, 2018.

. Dynamics of promoter bivalency and RNAP II pausing in mouse stem and differentiated cells. In: BMC developmental biology, (18), 1, pp. 2, https://doi.org/10.1186/s12861-018-0163-7, 2018.

. Insights into mammalian transcription control by systematic analysis of ChIP sequencing data. In: BMC bioinformatics, (19), Suppl 14, pp. 409, https://doi.org/10.1186/s12859-018-2377-x, 2018.

. DNA methylation signal has a major role in the response of human breast cancer cells to the microenvironment. In: Oncogenesis, (6), 10, pp. e390, https://doi.org/10.1038/oncsis.2017.88, 2017.

. Delineating biological and technical variance in single cell expression data. In: The International Journal of Biochemistry & Cell Biology, (90), pp. 161–166, https://doi.org/10.1016/j.biocel.2017.07.006, 2017.

Recent & Upcoming Talks

Contact

  • guillaume.devailly@inra.fr
  • GenPhySE, 24 chemin de Borde-Rouge - Auzeville Tolosane, 31326 Castanet Tolosan, FRANCE