Every Tuesday from 10AM to 12PM in 26-04-03A room.
The HUB Team is happy to welcome you every Tuesday, from 10AM to 12AM, for Open Days short questions. Simply come with your data/questions/smile to the room 26-04-03A of Francois Jacob building.
C3BI Team
Date : Thursday 16th April 2015 – 2PM Location : Retrovirus room – Lwoff building – ground floor Speakers : Bernd JAGLA
A potential list of topics to be discussed during these meetings :
– Recent papers related to this subject (see e.g. http://www.biomedcentral.com/1471-2164/16/97) – Difference between the different versions of the genomes and annotations – How to handle reads (from a sequencing machine) that align to multiple places in the genome – How to handle different individuals (e.g. from sequencing multiple patients), from a reference genome point of view – How to deal with transcripts / differential analysis of splice variants.
C3BI
Every Tuesday from 10AM to 12PM in 26-04-03A room.
The HUB Team is happy to welcome you every Tuesday, from 10AM to 12AM, for Open Days short questions. Simply come with your data/questions/smile to the room 26-04-03A of Francois Jacob building.
C3BI Team
Every Tuesday from 10AM to 12PM in 26-04-03A room.
The HUB Team is happy to welcome you every Tuesday, from 10AM to 12AM, for Open Days short questions. Simply come with your data/questions/smile to the room 26-04-03A of Francois Jacob building.
C3BI Team
Date : 2nd April 2015 – 11 AM Location : Salle Jean-Paul Aubert, ground floor Building Fernbach Speakers : Franck Picard – Laboratoire de Biométrie et Biologie Evolutive, Université Claude Bernard – Lyon
Abstract
Replication is the mechanism by which genomes are duplicated into two exact copies. Genomic stability is under the control of a spatiotemporal program that orchestrates both the positioning and the timing of firing of about 50,000 replication starting points, also called replication origins. Replication bubbles found at origins have been very difficult to map due to their short lifespan. Moreover, with the flood of data characterizing new sequencing technologies, the precise statistical analysis of replication data has become an additional challenge. We propose a new method to map replication origins on the human genome, and we assess the reliability of our finding using experimental validation and comparison with origins maps obtained by bubble trapping.
This fine mapping then allowed us to identify potential regulators of the replication dynamics. Our study highlights the key role of CpG Islands and identifies new potential epigenetic regulators (methylation of lysine 4 on histone H4, and tri-methylation of lysine 27 on histone H3) whose coupling is correlated with an increase in the efficiency of replication origins, suggesting those marks as potential key regulators of replication. Overall, our study defines new potentially important pathways that might regulate the sequential firing of origins during genome duplication.
C3BI Team
Date : April, Thursday 9th – 2PM Location : Retrovirus room – André LWOFF building Speekers: Valentine Murigneux, in Lymphocyte Development & Oncogenesis group, led by Ludovic Deriano
Uncovering Somatic Mutations in Genomically Unstable Mouse Lymphomas using Next-Generation Sequencing Technologies.
Genomic instability is a hallmark of many cancer cells and is thought to lead to the rapid evolution of subclones that are then selected for invasiveness, metastatic potential, and drug resistance. Specifically, failure to properly repair DNA double strand breaks can lead to complex chromosomal and genomic rearrangements characteristic of many cancers. In this study, using next generation sequencing technologies, we have analyzed the genomes and transcriptomes of T cell lymphomas originating from a series of genetically modified mouse models that carry specific deficiencies in genes maintaining genome stability during the physiological process of V(D)J recombination. We have developed bioinformatic pipelines to identify somatic mutations from whole-genome sequencing and RNA-sequencing. We have identified a set of tumor-specific variants (single nucleotide, copy number and structural variants), revealing the tumor landscape of V(D)J recombinase-induced lymphomas.
C3BI Team
