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RNASeq to investigate ETV4 and ETV5 function in human foetal lung tip progenitor cells

ABSTRACT: In order to understand transcription factor ETV4 and ETV5 function, we have knocked down ETV4 and ETV5 synergistically in human foetal lung tip progenitor organoids using an inducible CRISPRi system. We discovered that ETV double knockdown led to organoid cell self-renewal defects

ORGANISM(S): Homo sapiens

PROVIDER: GSE207179 | GEO | 2022/07/02

REPOSITORIES: GEO

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RNASeq to investigate ETV4 and ETV5 function in human foetal lung tip progenitor cells

Project description:RNASeq to investigate ETV4 and ETV5 function in human foetal lung tip progenitor cells

| PRJNA854069 | ENA

Targeted DamID to understand transcription factor genomic occupancy in human foetal lung progenitor cells

Project description:In order to study the genomic occupancy of transcription factors, including SOX9, ETV4 and ETV5, in human foetal lung tip progenitor cells, we have introduced Targeted DamID system via lentivirus in a human foetal lung tissue derived organoid culture (Nikolic et al., 2017). We were able to identify the corresponding TF motif enrichment and discovered a potential co-regulation function of SOX9 and ETV factors in human feotal lung progenitor cells. This study has pioneered the use of targeted DamID approach in tissue derived organoid system.

2022-04-30 | GSE189786 | GEO

Chip-chip from Mouse E11.5 distal limb tissue cells for Gabpa, Ets1, Elf1, Etv4, Etv5 antibody

Project description:Two different groups of Ets transcription factors differentially act directly at the ZRS to define the spatial expression of Shh in the limb. Chromatin immunoprecipitation (ChIP) of Gabpa, Ets1, Etv4, Etv5 and Elf1 and by ChIP-on-chip analysis demonstrated that with the exception of Elf1 all bind directly to the Shh limb enhancer, the ZRS. Array design includes 2 biological replicates for Gabpa and Elf1, and two biological replicates and one dye swap replicate for Ets1, Etv4 and Etv5 samples.

2012-02-01 | E-GEOD-33997 | biostudies-arrayexpress

Transcription profiling of mouse knockouts for Etv4 and Etv5 - plusGDNF and minusGDNF comparison using U74Av2 and 430A arrays

Project description:GDNF signaling through the Ret receptor tyrosine kinase is critical for ureteric bud branching morphogenesis during kidney development yet few of the downstream genes are currently known. We find that the ETS transcription factors Etv4 and Etv5 are positively regulated by Ret signaling in ureteric bud tips. Etv4-/-Etv5+/- mice display either renal agenesis or severe hypodysplasia, while kidney development fails completely in double homozygotes. We identify several genes whose expression in the ureteric bud depends on Etv4 and Etv5, including Cxcr4, Myb, Met, Mmp14. Thus, Etv4 and Etv5 are key components of a gene network downstream of Ret that promotes and controls renal branching morphogenesis. Experiment Overall Design: 3 plus GDNF and 2 minus GDNF chips were analyzed with different pooled samples for each chip (U74Av2 and 430A). Sample comparisons and statistical analysis were performed using dChip 1.3, using the Comparison Analysis feature to identify genes differentially expressed between the two groups. The following filtering criteria were used: the “lower limit” for fold-change between the means of the +GDNF and -GDNF samples must exceed 1.2 with a 90% confidence limit, and the absolute difference between the two group means must exceed 100.

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Etv4 and Etv5 binding sites in EpRas mouse mammary gland epithelial cell line [ChIP-seq]

Project description:We searched for roles of Etv4 and Etv5 during EMT through genome-wide analysis of their binding sites in Ras-transformed mammary gland epithelial cells.

2017-04-10 | GSE89618 | GEO

Chip-chip from Mouse E11.5 distal limb tissue cells for Gabpa, Ets1, Elf1, Etv4, Etv5 antibody

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Murine ES Cells: Control vs. ETV4/5 double KO

Project description:ETS-related transcription factors ETV4 and ETV5 play crucial roles for organogenesis and morphogenesis. We compared the transcriptional profiles between wild-type and ETV4 and ETV5 double knockout (ETV4/5 dKO) ES cells by an oligo DNA microarray analysis. Self-renewal capacity and pluripotency are known to be controlled by an ES cell-specific transcription factor network; therefore, we focused on transcription-associated genes. Of 1258 transcription-related genes, 47 genes were significantly downregulated and 98 genes were significantly upregulated in ETV4/5 dKO ES cells. Several genes whose expression is specific to undifferentiated ES were repressed in ETV4/5 dKO ES cells. In contrast, expression of differentiation markers was enhanced in ETV4/5 dKO ES cells.

2015-09-13 | GSE47225 | GEO

Gene expression changes upon knockdown or over-expression of the ETS gene ETV4 in prostate cancer cell lines

Project description:Chromosomal abnormalities that give rise to elevated expression levels of the ETS genes ETV1, ETV4, ETV5, or ERG are prevalent in prostate cancer, but the function of these transcription factors in carcinogenesis is not clear. Previous work implicates ERG, ETV1, and ETV5 as regulators of invasive growth but not transformation in cell lines. Here we show that the PC3 prostate cancer cell line provides a model system to study the over-expression of ETV4. Anchorage independent growth assays and microarray analysis indicate that high ETV4 expression is critical for the transformation phenotype of PC3 cells. However, genes up-regulated upon ETV4 over-expression were very similar to genes up-regulated by ETV1 over-expression in the RWPE-1 normal prostate cell line. Together these data indicate that the ETV4 dependent transformation phenotype observed in PC3 cells is due to the genetic background of the cell line, rather than a distinct characteristic of ETV4. Furthermore, these findings suggest that the function of ETS genes in prostate cancer may differ based on other genetic alterations in a tumor. Two sets of two color experiments. First is PC3 cells expressing one of two independent ETV4 shRNAs versus PC3 cells expressing a control shRNA (luciferase). Second is RWPE-1 cells expressing 3xFlag tagged ETV4 versus RWPE-1 cells with a control (empty) vector.

2011-03-24 | E-GEOD-21209 | biostudies-arrayexpress

Gene expression changes upon knockdown or over-expression of the ETS gene ETV4 in prostate cancer cell lines

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The transcription factors Etv4 and Etv5 mediate formation of the ureteric bud tip domain during kidney development.

Project description:Signaling by the Ret receptor tyrosine kinase promotes cell movements in the Wolffian duct that give rise to the first ureteric bud tip, initiating kidney development. Although the ETS transcription factors Etv4 and Etv5 are known to be required for mouse kidney development and to act downstream of Ret, their specific functions are unclear. Here, we examine their role by analyzing the ability of Etv4 Etv5 compound mutant cells to contribute to chimeric kidneys. Etv4(-/-);Etv5(+/-) cells show a limited distribution in the caudal Wolffian duct and ureteric bud, similar to Ret(-/-) cells, revealing a cell-autonomous role for Etv4 and Etv5 in the cell rearrangements promoted by Ret. By contrast, Etv4(-/-);Etv5(-/-) cells display more severe developmental limitations, suggesting a broad role for Etv4 and Etv5 downstream of multiple signals, which are together important for Wolffian duct and ureteric bud morphogenesis.

| S-EPMC2875840 | biostudies-other

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