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Differential gene expression analysis of colonic epithelial cells from wildtype and PRMT5 heterozygote mice

ABSTRACT: Differential gene expression analysis of colonic epithelial cells from wildtype and PRMT5 heterozygote mice

PROVIDER: PRJNA915003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22863550_1.fastq.gz	Fastqsanger.gz
	SRR22863550_2.fastq.gz	Fastqsanger.gz
	SRR22863551_1.fastq.gz	Fastqsanger.gz
	SRR22863551_2.fastq.gz	Fastqsanger.gz
	SRR22863552_1.fastq.gz	Fastqsanger.gz

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Differential gene expression analysis of colonic epithelial cells from wildtype and PRMT5 heterozygote mice

Project description:PRMT5 is a type II arginine methyltransferase enzyme that is abundantly expressed in intestinal epithelial cells (IECs) of the colon. Here, we compared the transcriptome of the colonic epithelium from wildtype and PRMT5 heterozygote mice under steady state. We found that PRMT5-regulated genes are involved in anti-microbial responses and immune signaling.

2023-09-04 | GSE221566 | GEO

PRMT5 protects genomic integrity during global DNA demethylation in primordial germ cells and preimplantation embryos

Project description:Primordial germ cells (PGCs) and preimplantation embryos undergo epigenetic reprogramming, which entails comprehensive erasure of DNA methylation. We found that PRMT5, an arginine methyltransferase, translocates from the cytoplasm to the nucleus during this process. Here we show that conditional loss of PRMT5 in early PGCs caused complete male and female sterility, which is preceded by upregulation of LINE1 and IAP transposons and DNA damage response. Similarly, loss of maternal-zygotic PRMT5 also leads to IAP upregulation and early embryonic lethality. We detected the PRMT5-catalysed repressive H2A/H4R3me2s modification on LINE1 and IAP in early wildtype PGCs, directly implicating this mark in the maintenance of transposon silencing during DNA hypomethylation. PRMT5 subsequently translocates back to the cytoplasm of PGCs to participate in the previously described PIWI-interacting RNA (piRNA) pathway that promotes transposon silencing via de novo DNA re-methylation. Thus, PRMT5 has a novel direct role in genome defense during preimplantation development and in PGCs at the time of global DNA demethylation PGCs mRNA profiles of embryonic day 11.5 dpc control (Blimp1Cre;Prmt5flox/+) and Prmt5 germ cell knockout (Blimp1Cre;Prmt5 flox/flox) were generated by deep sequencing (SOLiD next generation sequencing).

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PRMT5 protects genomic integrity during global DNA demethylation in primordial germ cells and preimplantation embryos

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PRMT5 is essential for sustaining normal adlut hematopoiesis

Project description:Examining the effects of PRMT5 loss on the gene expression profile of hematopoietic stem and progenitor cells We established the PRMT5 conditional KO mice, and bred the mice with Mx1 cre transgenic mice to delete PRMT5 in hematopoietic cells. We isolated hematopoetic stem and progenitor cells 3 days after PRMT5 deletion, and examined the gene expression files using RNA-sequencing.

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Differential expression of microRNA in Muc2-/- mouse colonic epithelial cells

Project description:Intestinal epithelia are protected by a layer of mucin secreted by goblet cells against mechanical and chemical injuries, potent causes of inflammation, and the most abundant secreted intestinal mucin is encoded by the Muc2 gene. Genetic deletion of Muc2 causes intestinal inflammation in early stage and tumors after 3 months. The underlying mechanisms are not clear, but epigenetic alterations, particularly, up- and down-regulated microRNAs are involved in the malignant transformation from colitis to cancer. We used miRNA array to profile the differential expression of the miRNAs in Muc2-/- mouse colonic epithelial lin comparison with those in wild-type mice. Total RNA were extracted from mouse colonic epithelial cells and Muc2-/- and +/+, and the RNA were hybridized on Affymetrix miRNA microarray to determine the alterations of miRNAs during colitis development and its malignant transformation from colitis to cancer. To the end, we found miRNA were differential expressed in the Muc2-/- mice, among them 20 miRNAs were significantly downregulated and 71 miRNAs were significantly upregulated in Muc2-/- mice, in comparison with Muc2+/+ mice (change fold >2 or <0.5; T<0.01, p value< 0.05, q value< 0.05).

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ChIP-on-chip from MDA-MB-231 cells with PHF1, CUL4B and PRMT5

Project description:It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells. comparison of PHF1, CUL4B and PRMT5 target genes

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