Project description:Hi-C experiment was performed to map and compare potential evolutionary changes in chromatin structural organisation of human, chimpanzee and macaque iAstrocytes.
Project description:H3K27ac ChIP-Seq experiment was performed to map and compare potential changes in elements of mouse embryonic stem cells and their derived neural stem cells
Project description:CTCF ChIP-Seq experiment was performed to map and compare potential changes of CTCF binding, in mouse embryonic stem cell and ES derived neural stem cells.
Project description:Human SGBS preadipocytes were differentiated into adipocytes, and human iPSCs were differentiated into hypothalamic neurons. Cells were collected for in situ promoter capture Hi-C [PMID: 29988018] at several differentiation stages. The differentiations were performed in one biological replicate, with two technical replicates (different wells of the differentiation that were also processed individually during library preparation). SGBS Day0: Represents the preadipocyte state. SGBS Day2: Represents immature adipocytes. SGBS Day8: Represents early mature adipocytes. SGBS Day16: Represents mature adipocytes. Hypothalamic Day 12: Represents early hypothalamic neurons. Hypothalamic Day 16: Represents mid hypothalamic neurons. Hypothalamic Day 27: Represents mature hypothalamic neurons.
Project description:We generated an interaction map using capture in situ Hi-C in human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by capture in situ Hi-C
Project description:Repair of DNA Double Strand Breaks produced in transcriptionally active chromatin occurs through a mechanism, Transcription-Coupled DSB repair (TC-DSBR), that is yet poorly characterized. Here, using a screening approach scoring multiple outputs in human cells, we identified the PER complex, a key module ensuring circadian oscillations, as a novel TC-DSBR player, being enriched at DSB occurring in transcribed loci, as compared to DSB induced in un-transcribed loci. We further found that PER2 contributes to target TC-DSBs at the nuclear envelope (NE) and to foster Rad51- mediated repair. PER2 deficiency triggers decreased DSB anchoring to NE, resulting in an increase of DSB clustering, checkpoint activation and translocation frequency. In agreement, we found that the circadian clock also regulates DSB anchoring to the NE, checkpoint activation, and HR usage. Our study provides a direct link between the circadian clock and the response to DNA Damage, opening new therapeutic strategies for chemotherapies based on topoisomerase poisons that induce DSBs in active loci.
Project description:We generated Hi-C interaction maps of iPSC and iPSC-derived cardiomyocytes as a resource to help identifying regulatory elements and their target genes in these tissues.
Project description:The DEAD-box ATP-dependent RNA helicases DDX5 and DDX17 play a role in many aspects of cellular RNA biology, including metabolism, translation, splicing, transcription regulation, ribosome biogenesis, mRNA nuclear export, and miRNA processing. Moreover, both RNA helicases were found to either promote or inhibit viral replication upon several RNA virus infections. Here we show that DDX5 depletion by siRNA or CRISPR/Cas9 has a negative impact on Sindbis virus (SINV) infection at the viral protein, RNA and infectious particle level. Moreover, we demonstrate that DDX5 which is predominately nuclear in uninfected conditions, re-localizes to the cytoplasm upon infection where it interacts with the viral RNA and with the SINV capsid protein. Furthermore, proteomic analysis of DDX5 interactome in mock and SINV infected HCT116 cells confirmed its interaction with DDX17 and identified PNPT1 as a new DDX5 partner. Of note, while PNPT1 localization remains mostly unchanged in mock and infected cells, DDX17 re-localizes to the cytoplasm with DDX5 upon SINV infection and interacts with SINV capsid protein. Finally, depletion of DDX17 further reduces SINV infection in a DDX5-depleted background suggesting a cumulative proviral effect of DDX5 and 17 proteins on SINV.