ABSTRACT: Gene expression comparison between different stages of endogenous Sertoli cells and induced embryonic Sertoli cells derived from MEFs and TTFs
Project description:To compare the transcriptional profile of endogenous Sertoli cells from different Stage of Sertoli cell development (embryonic, immature, mature) to the transcriptionla profile of induced embryonic Sertoli cells derived from MEFs or TTFs we employed the agilent whole genome microarray Keywords: Expression profiling by array
Project description:To compare the transcriptional profile of endogenous Sertoli cells from different Stage of Sertoli cell development (embryonic, immature, mature) to the transcriptionla profile of induced embryonic Sertoli cells derived from MEFs or TTFs we employed the agilent whole genome microarray Keywords: Expression profiling by array The following samples were analyzed in duplicates (MEFs, TTFs, ieSCs (derived from MEFs), ieSCs (derived from TTFs), 14.5 dpc male gonad, immature Sertoli (19 dpc embryo testis) and mature (8 week-old mouse testis))
Project description:To compare the the genomic profile of MEFs, immature Sertoli, mature Sertoli cells, and MEFs (NWD) after infection of Nr5a1, Wt1 and Dmrt1 after 1 month of dox exposure.
Project description:Cellular interactions between germ cells and gonadal somatic cells are essential for the progression of gametogenesis. Here, we report a culture method for generating fetal testicular somatic cell–like cells (fTeSLCs) from embryonic stem cells. These fTeSLCs exhibit a transcriptomic profile closely resembling that of their in vivo counterparts, including distinct cell populations corresponding to Sertoli cells and interstitial cells. For functional assessment, interstitial cell–like cells (ICLCs) and Sertoli-like cells (SerLCs) were isolated from fTeSLCs. ICLCs differentiated into Leydig cells when cocultured with testes lacking endogenous Leydig cells, thereby restoring androgenic support. SerLCs reconstituted the seminiferous epithelium following selective ablation of endogenous Sertoli cells. Both cell types supported spermatogenesis and generated spermatids reaching the elongating stage. Notably, round spermatids derived from these reconstructed systems produced viable offspring by round spermatid injection. These findings demonstrate that fTeSLCs can generate functional testicular somatic cells, providing a valuable platform for studying testis development and spermatogenesis.
Project description:To compare the the genomic profile of MEFs, immature Sertoli, mature Sertoli cells, and MEFs (NWD) after infection of Nr5a1, Wt1 and Dmrt1 after 1 month of dox exposure. MEFs (NWD) were infected with Nr5a1, Wt1 and Dmrt1 and were exposed to dox for 1 month. MEFs, immature Sertoli and mature Sertoli cells were cultured for 3 days and collected
Project description:To compare the the genomic profile of MEFs and induced embryonic Sertoli-like cells following 2 weeks of dox withdrawal. ieSCs (from MEFs and from TTFs) and MEF control were grown in F12/DMEM medium without dox for two weeks.
Project description:Post-translational modification by SUMO is a key regulator of cell identity. In mouse embryonic fibroblasts (MEFs), SUMO impedes reprogramming to pluripotency, while in embryonic stem cells (ESCs), it represses the emergence of totipotent-like cells, suggesting that SUMO targets distinct substrates to preserve somatic and pluripotent states. Using MS-based proteomics, we show that the composition of endogenous SUMOylomes differs dramatically between MEFs and ESCs. In MEFs, SUMO2/3 targets proteins associated with canonical SUMO functions, such as splicing, and transcriptional regulators driving somatic enhancer selection. In contrast, in ESCs, SUMO2/3 primarily modifies highly interconnected repressive chromatin complexes, thereby preventing chromatin opening and transitioning to totipotent-like states. We also characterize several SUMO-modified pluripotency factors and show that SUMOylation of Dppa2 and Dppa4 impedes the conversion to 2-cell-embryo-like states. Altogether, we propose that rewiring the repertoire of SUMO target networks is a major driver of cell fate decision during embryonic development.
