Le jeudi 5 et vendredi 6 juillet, le Centre de Bioinformatique de Bordeaux (CBiB) organise un atelier autour de l'exploitation de données génomiques, s'adressant aux biologistes et bioinformaticiens. Cet atelier sur deux jours se composera de deux séminaires et d'un tutorial Galaxy.
Séminaire de Anton Nekrutenko (http://bmb.psu.edu/directory/aun1) University Park, Pennsylvania,USA. Jeudi 5 juillet à 11h, Salle de Conférences du Centre de Génomique Fonctionnelle Bordeaux (CGFB), Université Bordeaux Segalen
Continuing evolution of DNA sequencing has transformed modern biology. Areas of life science research that were previously distant from each other in ideology, analysis practices, and toolkits such as microbial ecology and personalized medicine or conservation biology and cell and molecular biology have all embraced techniques that rely on next generation sequencing (NGS) instruments. These rapid and dramatic developments have enabled researchers to design and implement studies that were unthinkable just a few years ago. Yet the capacity to generate the data greatly outpaces our ability to analyze it. Existing sequencing technologies are much more mature and accessible than the methodologies for individual researchers to move, store, analyze, and present data in a fashion that is transparent and reproducible. Although this phenomenon is only natural - sequencing technologies advanced so rapidly that the analytical approaches simply have not had time to catch up - life sciences have reached a pivotal point where scalable and widely available analysis solutions are needed to truly achieve progress and move the field forward. Here we discuss currently pressing issues, discuss promising solutions, and venture into potential future developments.
Anton Nekrutenko est le "Principal Investigator" de GALAXY ( http://galaxy.psu.edu/), plate-forme largement utilisée par la communauté de biologistes et bioinformaticiens pour développer des work-flows d'analyses de données moléculaires à haut débit.
Un tutorial pour Bioinformaticiens et Biologistes à l'utilisation de la bioinformatique (tutorial d'environ 3 heures sur ordinateur avec pause café au milieu) sera organisé le jeudi 5 juillet de 14h-18h, Salle de Conférences du Centre de Génomique Fonctionnelle Bordeaux (CGFB), Université Bordeaux Segalen.
Séminaire de Kateryna Makova (http://www.bx.psu.edu/makova_lab/), Center for Comparative Genomics and Bioinformatics, Pennsylvania State University, University Park, Pennsylvania,USA.Vendredi 6 juillet à 11h, Salle de Conférences du Centre de Génomique Fonctionnelle Bordeaux (CGFB), Université Bordeaux Segalen
Chromosomal common fragile sites (CFSs) are unstable genomic regions that break under replication stress and are involved in structural variation. They frequently are sites of chromosomal rearrangements in cancer and of viral integration. However, CFSs are undercharacterized at the molecular level and thus difficult to predict computationally. Newly available genome-wide profiling studies provide us with an unprecedented opportunity to associate CFSs with features of their local genomic contexts. Here, we contrasted the genomic landscape of cytogenetically defined aphidicolin-induced CFSs (aCFSs) to that of nonfragile sites, using multiple logistic regression. We also analyzed aCFS breakage frequencies as a function of their genomic landscape, using standard multiple regression. We show that local genomic features are effective predictors both of regions harboring aCFSs (explaining ~77% of the deviance in logistic regression models) and of aCFS breakage frequencies (explaining ~45% of the variance in standard regression models). In our optimal models (having highest explanatory power), aCFSs are predominantly located in G-negative chromosomal bands and away from centromeres, are enriched in Alu repeats, and have high DNA flexibility. In alternative models, CpG island density, transcription start site density, H3K4me1 coverage, and mononucleotide microsatellite coverage are significant predictors. Also, aCFSs have high fragility when colocated with evolutionarily conserved chromosomal breakpoints. Our models are predictive of the fragility of aCFSs mapped at a higher resolution. Importantly, the genomic features we identified here as significant predictors of fragility allow us to draw valuable inferences on the molecular mechanisms underlying aCFSs.