Project description:We have used ATAC-seq to track cell state changes that occur during the differentiation of mouse embryonic stem cells to defined neural progenitor fates. We have performed ATAC-seq every 24 hours in cells en route to 3 distinct neural progenitors fates, anterior, hindbrain and spinal cord. This has allowed us to define how cells transition to a neural state, based on their enhancer usage. We identified regions distinct to different anterior-posterior neural progenitors, and validated their relevance by performing in vivo ATAC-seq on neural progenitors isolated from different axial levels of mouse embryos.
Project description:SAGA and ATAC are two related transcriptional coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development but the precise role of the two complexes in RNA polymerase II transcription in mammals is less understood. To determine whether SAGA and ATAC have redundant or specific functions dependent on their HAT activities, we compared the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC subunits are required for complex assembly, mouse ESC growth and self-renewal. Additionally, ATAC, but not SAGA subunits are required for ESC viability by regulating the transcription of translation-related genes. Surprisingly, depletion of specific or shared HAT module subunits caused a global decrease in histone H3K9 acetylation, but did not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for viability and self-renewal of mouse ESCs by regulating transcription through different pathways, in a HAT-independent manner.
Project description:We have generated ATAC-sequencing datasets of the regulome of mouse neural stem and progenitor cells derived from embryonic stem cells, with allele-specific deletions of Sox2 enhancer cluster regions. ATAC-seq experiments were conducted to evaluate the alterations in chromatin accessibility at candidate regulatory elements genome-wide in neural stem and progenitor cells with Sox2 enhancer loss-of-function.
Project description:Chromatin accessibility was profiled by ATAC-seq in normal and glioblastoma-derived neural stem (GNS) cells, in self-renewing conditions and in response to differentiation stimulus with bone morphogenic protein (BMP).
Project description:Cells were isolated from mouse embryonic neural crest stem cells at culture day 2 (NCSC), from day 7 in vitro differentiated progeny (NCP) and day 2 epidermal neural crest stem cells from bulge explants of adult whisker follicles (EPI-NCSC). Keywords: LongSAGE embryonic neural crest stem cells at culture day 2 (NCSC), from day 7 in vitro differentiated progeny (NCP) and day 2 epidermal neural crest stem cells from bulge explants of adult whisker follicles (EPI-NCSC).