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RNA seq after RNA pol III manipulation by Brf1 and Maf1 knockdown, Maf1 overexpression and ML60218 treatment in ST2 cells before, and during differentiation into osteoblasts

ABSTRACT: RNA seq after RNA pol III manipulation by Brf1 and Maf1 knockdown, Maf1 overexpression and ML60218 treatment in ST2 cells before, and during differentiation into osteoblasts

PROVIDER: PRJNA839399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19271400_1.fastq.gz	Fastqsanger.gz
	SRR19271400_2.fastq.gz	Fastqsanger.gz
	SRR19271401_1.fastq.gz	Fastqsanger.gz
	SRR19271401_2.fastq.gz	Fastqsanger.gz
	SRR19271402_1.fastq.gz	Fastqsanger.gz

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RNA seq after RNA pol III manipulation by Brf1 and Maf1 knockdown, Maf1 overexpression and ML60218 treatment in ST2 cells before, and during differentiation into osteoblasts

Project description:Maf1, a key repressor of RNA polymerase III-mediated transcription, has been shown to promote mesoderm formation in vitro. Here, we show, for the first time, that Maf1 plays a critical role in the regulation of osteoblast differentiation. We also found that, in contrast to MAF1 overexpression, other perturbations that repress RNA pol III transcription, including Brf1 knockdown and the chemical inhibition of RNA pol III by ML-60218, inhibited osteoblast differentiation. RNA-seq was used to determine the basis for these opposing actions on osteoblast differentiation. RNA polymerase III-dependent transcription was manipulated in ST2 stromal cells by Brf1 or Maf1 knockdown, ML-60218 treatment and MAF1 overexpression. The ST2 cells were then tested for their capacity to differentiate into osteoblasts. RNA-seq was performed on day 0, before differentiation and day 4 after differentiation medium was added. The modalities used to perturb RNA pol III transcription resulted in distinct changes gene expression, indicating that this transcription process is highly sensitive and triggers diverse gene expression programs and phenotypic outcomes. Specifically, Maf1 induced genes in ST2 cells known to promote osteoblast differentiation. Furthermore, genes that are induced during osteoblast differentiation displayed codon bias.

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MAF1 Represses CDKN1A through a Pol III-Dependent Mechanism

Project description:MAF1 represses Pol III-mediated transcription by interfering with TFIIIB and Pol III. Herein, we found that MAF1 knockdown induced CDKN1A transcription and chromatin looping concurrently with Pol III recruitment. Simultaneous knockdown of MAF1 with Pol III or BRF1 (subunit of TFIIIB) diminished the activation and looping effect, which indicates that recruiting Pol III was required for activation of Pol II-mediated transcription and chromatin looping. ChIP analysis after MAF1 knockdown indicated enhanced binding of Pol III and BRF1, as well as of CFP1, p300, and PCAF, which are factors that mediate active histone marks, along with the binding of TBP and POLR2E to the CDKN1A promoter. Simultaneous knockdown with Pol III abolished these regulatory events. Similar results were obtained for GDF15. Our results reveal a novel mechanism by which MAF1 and Pol III regulate the activity of a protein-coding gene transcribed by Pol II. Knockdown assay was performed using siRNA obtained from MISSION®RNA (Sigma). Inhibition of expression of Pol III (SASI_Hs01_00046568) and MAF1 (SASI_Hs01_00135954) was achieved by transfection with LipofectamineTM RNAiMax (Invitrogen) according to the manufacturer’s protocol. MISSION® siRNA Universal Negative Control (Sigma) was used as knockdown control. Cells were transfected in serum-free medium. After 8 h, the siRNA containing medium was replaced with complete medium.

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Pairwise comparison of ST2+ and ST2- FOXP3+ T cells derived from mouse intestinal tumors

Project description:Colorectal cancer (CRC) was induced in Foxp3/eGFP reporter mice by the azoxymethane/dextran sulphate sodium salt (AOM/DSS) protocol. Mice were injected i.p. with the procarcinogen AOM (12.5 mg/kg of body weight). After 1 week, mice received drinking water supplemented with 2.5% DSS for 5 to 7 days, followed by 2 weeks of regular water. The DSS administration was repeated twice with 2% DSS. Mice were sacrificed at week 11 and lamina propia lymphocytes (LPLs) from the colon were isolated. CD4+FOXP3+ (eGFP+) ST2+ or ST2- Tregs were separated from colonic LPLs of CRC induced mice using a FACSAria II cell sorter. Microarray analysis was performed to analyze if ST2+ FOXP3+ Tregs from the colon of CRC mice present a distinct transcription pattern compared to ST2- FOXP3+ Tregs. By this, the role of ST2 for Treg function during intestinal tumorigenesis should be characterized.

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Maf1 chromatin immunodepletion upon rapamycin treatment

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