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RNA-Seq analysis in human trophoblast stem cells (CT27) upon depletion of transcription factor GATA2 or GATA3

ABSTRACT: The GATA transcription factors, particularly GATA2 and GATA3 are responsible for trophoblast stem cells self renewal and differentiation in mice. However, we have a poor understanding about the contribution of GATA2 and GATA3, in the trophoblast cells in humans. Thus, the goal of this study is to define the importance of GATA factors in orchestrating global gene expression program in human trophoblast stem cells. Using a RNA interference strategy (RNAi), we depleted GATA2 or GATA3 expression in human trophoblast stem cells (GATA2 KD or GATA3 KD) . We then differentiated GATA2 KD and GATA3 KD human trophoblast stem cells into syncytiotrophoblasts(SynT) and compared global gene expression patterns via RNA sequencing (RNA-seq). Three individual experiments were performed for the differentiated SynT state. The submitted files contain the data (raw fastq files, count data and deseq2 output) from those experiments.

ORGANISM(S): Homo sapiens

PROVIDER: GSE214634 | GEO | 2024/01/26

REPOSITORIES: GEO

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Project description:Transcriptional profiling of mouse comparing in vitro-derived DC progenitors from control and Gata2 conditional knockout mice. Two-condition experiment, Control DCs vs. G2 Knockout DCs. Biological replicates: 4 control, 3 Gata2 knockout, independently grown and harvested. One replicate per array. Dendritic cells (DCs) are critical immune response regulators; however, the mechanism of DC differentiation is not fully understood. Heterozygous germline GATA2 mutations induce GATA2 deficiency syndrome, characterized by monocytopenia, a predisposition to myelodysplasia/acute myeloid leukemia, and a profoundly reduced DC population, which is associated with increased susceptibility to viral infections, impaired phagocytosis, and decreased cytokine production. To define the role of GATA2 in DC differentiation and function, we studied Gata2 conditional knockout and haploinsufficient mice. Gata2 conditional deficiency significantly reduced the DC count, whereas Gata2 haploinsufficiency did not affect this population. GATA2 was required for the in vitro generation of DCs from Linâ??Sca-1+Kit+ cells, common myeloid-restricted progenitors, and common dendritic cell precursors, but not common lymphoid-restricted progenitors or granulocyte-macrophage progenitors, suggesting that GATA2 functions in the myeloid pathway of DC differentiation. Moreover, expression profiling demonstrated reduced expression of myeloid-related genes, including mafb, and increased expression of T-lymphocyte-related genes, including Gata3 and Tcf7, in Gata2-deficient DC progenitors. In addition, GATA2 was found to bind an enhancer element 190-kb downstream region of Gata3, and a reporter assay exhibited significantly reduced luciferase activity after adding this enhancer region to the Gata3 promoter, which was recovered by GATA sequence deletion within Gata3 +190. These results suggest that GATA2 plays an important role in cell fate specification toward the myeloid versus T lymphocyte lineage by regulating lineage-specific transcription factors in DC progenitors, thereby contributing to DC differentiation.

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RNA-Seq analysis in human trophoblast stem cells (CT27) upon depletion of transcription factor GATA2 or GATA3

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