Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CMTR1 is recruited to transcription start sites and has enhanced influence over ribosomal protein and histone genes [ChIP-seq]

ABSTRACT: We investigated the gene-specificity of mRNA cap methyltransferase CMTR1 and its impact in RNA expression. In this ChIP-seq experiment, we investigated the genome-wide chromatin binding profiles of CMTR1 in mouse embryonic stem cells. We demontrated that CMTR1 binds to the transcription start site (TSS) correlating with RNA polymerase II (RNAP II) levels, with predominant binding at histone genes and ribosomal protein (RP) genes. Moreover, the repression of CMTR1 expression resulted in a loss of RNAP II binding at the TSS.

ORGANISM(S): Mus musculus

PROVIDER: GSE175628 | GEO | 2022/02/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CMTR1 is recruited to transcription start sites and has enhanced influence over ribosomal protein and histone genes [RNA-seq]

Project description:We investigated the gene-specificity of mRNA cap methyltransferase CMTR1 and its impact in RNA expression. In this RNA-seq experiment, we used siRNA to knockdown the endogenous CMTR1 protein to investigate its role in mouse embryonic stem cells. We demonstrated that the repression of CMTR1 expression resulted in a loss of RNA expression, particularly of histone and ribosomal protein genes.

2022-02-25 | GSE175629 | GEO

CK2 phosphorylation of cap methyltransferase CMTR1 promotes RNAPII interaction

Project description:We investigated influence of CMTR1 phosphorylation by CK2 on RNA expression. In this experiment, we added wild-type and phosphorylation deficient mutant of CMTR1 and knocked out the endogenous CMTR1. We demonstrated that lack of phosphorylation of CMTR1 affects only small but specific group of genes.

2024-06-24 | GSE200103 | GEO

CMTR1 promotes colorectal cancer cell growth and immune evasion by transcriptionally regulating STAT3

Project description:CMTR1, also called IFN-stimulated gene 95 kDa protein (ISG95), is elevated by viral infection in a variety of cells. However, the function of CMTR1 in colorectal cancer (CRC), especially its role in tumorigenesis and immune regulation, remains unclear. Here, we first identified CMTR1 as a novel oncogene in colorectal cancer. Based on The Cancer Genome Atlas (TCGA) database exploration and human tissue microarray (TMA) analysis, we found that CMTR1 expression was markedly higher in colorectal cancer tissues compared to that in adjacent normal tissues. High CMTR1 was correlated with poor prognosis of colorectal cancer patients. Knockdown (KD) of CMTR1 significantly suppressed cell proliferation and tumorigenicity both in vitro and in vivo, whereas overexpression of CMTR1 exhibited the opposite effects. KEGG analysis revealed that the JAK/STAT signaling pathway was differentially enriched in colorectal cancer cells with CMTR1 KD. Mechanistically, repression of CMTR1 influenced RNAPII recruitment to the TSS and repression of STAT3 expression and activation. Furthermore, PD1 blockade immunotherapy was prominently enhanced with CMTR1 KD by increased infiltration of CD8+ T cells into tumor microenvironment. Overall, it appears that CMTR1 plays a key role in regulating tumor cell proliferation and antitumor immunity.

2023-04-12 | GSE220040 | GEO

DHX15 regulates CMTR1-dependent gene expression and cell proliferation

Project description:We discovered that the RNA helicase DHX15 is a regulator of the methyltransferase CMTR1. To determine the biological consequences of this interaction we overexpressed CMTR1 or a mutated CMTR1 (2LA)that does not bind DHX15, in the human breast cancer cell line HCC1806. To assess the effects of the DHX15-CMTR1 interaction on translation, polysomes were separated on a sucrose gradient and sequencing libraries generated from the polysomal and input RNA. We found that the DHX15-CMTR1 interaction controls ribosome loading of a subset of mRNAs and impacts on cell proliferation.

2018-06-05 | GSE113573 | GEO

CMTR1 is recruited to transcription start sites and promotes ribosomal protein and histone gene expression in embryonic stem cells.

Project description:CMTR1 (cap methyltransferase 1) catalyses methylation of the first transcribed nucleotide of RNAPII transcripts (N1 2'-O-Me), creating part of the mammalian RNA cap structure. In addition to marking RNA as self, N1 2'-O-Me has ill-defined roles in RNA expression and translation. Here, we investigated the gene specificity of CMTR1 and its impact on RNA expression in embryonic stem cells. Using chromatin immunoprecipitation, CMTR1 was found to bind to transcription start sites (TSS) correlating with RNAPII levels, predominantly binding at histone genes and ribosomal protein (RP) genes. Repression of CMTR1 expression resulted in repression of RNAPII binding at the TSS and repression of RNA expression, particularly of histone and RP genes. In correlation with regulation of histones and RP genes, CMTR1 repression resulted in repression of translation and induction of DNA replication stress and damage. Indicating a direct role for CMTR1 in transcription, addition of recombinant CMTR1 to purified nuclei increased transcription of the histone and RP genes. CMTR1 was found to be upregulated during neural differentiation and there was an enhanced requirement for CMTR1 for gene expression and proliferation during this process. We highlight the distinct roles of the cap methyltransferases RNMT and CMTR1 in target gene expression and differentiation.

| S-EPMC8934662 | biostudies-literature

To investigate gene expression changes in neurons lacking cap methyltransferase 1 (CMTR1)

Project description:Transcriptomic profiles of control and CMTR1-knockdown neurons.

2020-09-25 | GSE145223 | GEO

CMTR1 is recruited to transcription start sites and has enhanced influence over ribosomal protein and histone genes

Project description:CMTR1 is recruited to transcription start sites and has enhanced influence over ribosomal protein and histone genes

| PRJNA733118 | ENA

CLIP of mRNA capping enzyme CMTR1 in Drosophila melanogaster

Project description:The mRNA cap structure consists of the m7G "cap0" linked to the 5'-most nucleotide of the initial mRNA. The first two nucleotides of mRNA can be 2'-O-Ribose modified to form cap1 or cap2 structures. Here, mRNA was sequenced after CLIP with tagged recombinant CMTR1 and compared to input RNA.

2021-12-18 | GSE181321 | GEO

Piwi regulates the usage of alternative transcription start sites in the Drosophila ovary

Project description:Alternative transcription initiation, which refers to the transcription of a gene from different transcription start sites (TSSs), is prevalent in mammalian systems and has important biological functions. Although transcriptional regulation has been extensively studied, the mechanism that selects one TSS over others in a gene remains elusive. We discovered Piwi, an RNA-binding protein, regulated TSS usage of genes and identified 87 genes with significantly altered TSS usage (ATU) in piwi-deficient Drosophila ovaries using the cap-analysis gene expression sequencing (CAGE-seq) method. This regulation occurs in both germline and somatic cells in ovaries as well as in cultured ovarian somatic cells (OSCs). Correspondingly, RNA Pol II initiation and elongation at TSSs of ATU genes were affected in germline-piwi-knockdown ovaries and piwi-knockdown OSCs. We identified a FACT complex component, Ssrp, which is essential for mRNA elongation, as a novel interactor of Piwi in the nucleus. Temporally controlled knockdown of ssrp affected TSS usage of ATU genes whereas overexpression of ssrp partially rescued the TSS usage of ATU genes in piwi mutant ovaries. Thus, Piwi may interact with Ssrp to regulate TSS usage in Drosophila ovaries by affecting Pol II initiation and elongation.

2024-11-29 | GSE255438 | GEO

Piwi regulates the usage of alternative transcription start sites in the Drosophila ovary

2024-11-29 | GSE255440 | GEO