Project description:To investigate the role of the transcription factor AP-2 in craniofacial development, we performed: ATAC-seq on E11.5 craniofacial surface ectoderm in control and Tfap2a/Tfap2b ectoderm knock-out embryos; RNA-seq on E10.5 craniofacial prominences from control and Tfap2a/Tfap2b ectoderm knock-out embryos; histone-seq (H3K4me3) in E10.5 and E11.5 wild-type craniofacial surface ectoderm.
Project description:To investigate the role of the transcription factor AP-2 in craniofacial development, we performed: ATAC-seq on E11.5 craniofacial surface ectoderm in control and Tfap2a/Tfap2b ectoderm knock-out embryos; RNA-seq on E10.5 craniofacial prominences from control and Tfap2a/Tfap2b ectoderm knock-out embryos; histone-seq (H3K4me3) in E10.5 and E11.5 wild-type craniofacial surface ectoderm.
Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. Using a CRISPR/Cas9 approach, we generated three STAG2 knock-out isogenic clones (A673SA2m#1, TC71SA2m#1 and TC71SA2m#2) derived from A673 and TC71 STAG2 wild type (WT) Ewing sarcoma cell line. A STAG2 rescue model (A673_SA2r) generated by correcting the CRISPR mutation in the A673SA2m#1 model was also profiled using RNA-seq. Comparison of RNA-seq data allowed highlighting a broad transcriptional modulation upon STAG2 knock-out. In addition, we compared these analyses with STAG1 knock-out A673 derived model (A673SA1m#1) and with A673 (WT) and TC71 (WT) parental cells lines transfected with siCT or siEWS-FLI1.