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Profiling of histone modifications in GATA3 ZnFn2 mutant cells with progesterone treatment

ABSTRACT: Profiling of histone modifications in GATA3 ZnFn2 mutant cells with progesterone treatment

PROVIDER: PRJNA608968 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11189106_1.fastq.gz	Fastqsanger.gz
	SRR11189106_2.fastq.gz	Fastqsanger.gz
	SRR11189107_1.fastq.gz	Fastqsanger.gz
	SRR11189107_2.fastq.gz	Fastqsanger.gz
	SRR11189108_1.fastq.gz	Fastqsanger.gz

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Profiling of histone modifications in GATA3 ZnFn2 mutant cells with progesterone treatment

Project description:R330fs GATA3 mutant disrupts the progesterone network in T47D cells. We mapped active histone marks (H3K4me1 and H3K27ac) and repressive histone mark (H3K27me3) in the T47D GATA3 mutant cells after progesterone treatment. Control (vehicle) data has been posted under the accession number GSE130703.

2020-02-27 | GSE146008 | GEO

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Genome-wide analysis reveals unique regulation of transcription of Th2-specific genes by GATA3

Project description:Differentiation of naive CD4 T cells into type 2 helper (Th2) cells is accompanied by chromatin remodeling and increased expression of a set of Th2-specific genes including those encoding Th2 cytokines. IL-4-mediated STAT6 activation induces high levels of transcription of GATA3, a master regulator of Th2 cell differentiation, and enforced expression of GATA3 induces Th2 cytokine expression. However, it remains unclear whether the expression of other Th2-specific genes is induced directly by GATA3. A genome-wide unbiased ChIP-seq analysis revealed that GATA3 bound to 1,279 genes selectively in Th2 cells, and 101 genes in both Th1 and Th2 cells. Simultaneously, we identified 26 highly Th2-specific STAT6-dependent inducible genes by a DNA microarray analysis-based three-step selection processes, and among them 17 genes showed GATA3 binding. We assessed dependency on GATA3 for the transcription of these 26 Th2-specific genes, and 10 genes showed increased transcription in a GATA3-dependent manner while 16 genes showed no significant responses. The transcription of the 16 GATA3-nonresponding genes was clearly increased by the introduction of an active form of STAT6, STAT6VT. Therefore, although GATA3 has been recognized as a master regulator of Th2 cell differentiation, many Th2-specific genes are not regulated by GATA3 itself but in collaboration with STAT6. Th1 and Th2 subsets are profiled for mRNA expression Examination of GATA3-binding and 3 different histone modifications in Th1 and Th2 cells.

2011-03-31 | E-GEOD-28292 | biostudies-arrayexpress

Comparison of GATA3 mutant and GATA3 wild type isogenic MCF-7 and CAMA1 breast cancer cell lines

Project description:The GATA3 transcription factor is one of the most frequently mutated genes in breast cancer. Heterozygous mutations, largely frameshifting, are seen in 15% of estrogen receptor positive breast cancers, the subtype in which these mutations are almost exclusively found. Mouse studies have shown that Gata3 is critical for breast development and that GATA3 gene dosage affects breast tumor progression. Human patient data have shown that high Gata3 expression, a feature of luminal subtype breast cancers, is associated with a better prognosis. Although the frequency of GATA3 mutation suggests an important role in breast cancer development or progression, there is little understanding of how mutations in GATA3 affect its function in luminal breast epithelial cells and what gene expression changes result as a consequence of the mutations. Here, using gene editing, we have created two sets of isogenic human luminal breast cancer cell lines with and without a truncating GATA3 mutation. GATA3 mutation enhanced tumor growth in vivo but did not affect sensitivity to clinically used hormonal therapies or chemotherapeutic agents. We identified genes upregulated and downregulated in GATA3 mutant cells, a subset of which was concordantly differentially expressed in GATA3 mutant primary luminal breast cancers. Addback of mutant GATA3 recapitulated mutation-specific gene expression changes and enhanced soft agar colony formation, suggesting a gain of function for the mutant protein.

2018-01-12 | GSE101780 | GEO

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