Project description:Loss of the transcription factor Satb2 converts mouse colonic epithelium into an ileal type. Here, we report that Satb2 gene deletion alleviates SBS by replacing diminished absorptive function and by inducing lymphovascular channels in the proximal colon. Enhanced nutrient absorption following Satb2 loss increased body weight and survival of mice with SBS. Deletion of SATB2 by adeno-associated viral delivery of CRISPR Split Cas9 to human colon organoids, followed by xenotransplantation into mice, resulted in ileal morphology and expression of ileal marker genes. This approach offers a feasible strategy for future treatment of SBS.
Project description:The goal of the study was to identify the binding site of SATB2 in wild-ype cortex by performing ChIP-seq using SATB2 antibody. E15 cortical tissues were dissected, lysed and fixed. Chromatin was prepared by sonication. Sequences bound by SATB2 protein was precipitated using a SATB2 antibody. Sequencing was performed on Illumina Genome Analyzer II. SATB2 binding peaks were called using MACS. ChIP for Satb2, followed by sequencing on Illumina Genome Analyzer II platform
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. This SuperSeries is composed of the following subset Series: GSE17487: Expression data in WT and Satb1-/- ES cells GSE17488: Expression data in WT and ES cells overexpressing Satb1 GSE17489: Expression data in WT and ES cells overexpressing Satb2 Refer to individual Series
Project description:The goal of the study was to identify the binding site of SATB2 in wild-ype cortex by performing ChIP-seq using SATB2 antibody. E15 cortical tissues were dissected, lysed and fixed. Chromatin was prepared by sonication. Sequences bound by SATB2 protein was precipitated using a SATB2 antibody. Sequencing was performed on Illumina Genome Analyzer II. SATB2 binding peaks were called using MACS.
Project description:Satb1 and Satb2 are regulators of higher order chromatin in T cells and osteoblasts repectively. We were interested if Satb1 and Satb2 play a role in the regulation of gene expression in ES cells. ES cells which can inducibly express Satb1 or Satb2 were generated using the tet-ON system. In this experiment, we compared gene expression in uninduced cells to that in cells which had been induced for 24h to express Satb2 ectopcially at very high levels.
Project description:The goal of the study was to compare gene expression of P0 wild-type and P0 Satb2-/- cortices. Total RNAs were isolated from P0 cortices dissected from wild-type and Satb2-/- mice (n=3 for each genotype), following Qiagen RNAeasy kit instruction.Sequence libraries were made following Illumina RNA TruSeq library preparation guide.The libaries were pair-end sequenced (50nt per end). Differentially expressed genes were identified by DESEQ. Total RNAs were isolated from P0 cortices (3 control and 3 mutants), and sequenced on Illumina Genome Analyzer