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Transcriptome-wide m6A Methylation Profiling of Wild Type and ALKBH5-/- Peritoneal Macrophages by m6A-seq

ABSTRACT: Transcriptome-wide m6A Methylation Profiling of Wild Type and ALKBH5-/- Peritoneal Macrophages by m6A-seq

PROVIDER: PRJNA525142 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8655030_1.fastq.gz	Fastqsanger.gz
	SRR8655030_2.fastq.gz	Fastqsanger.gz
	SRR8655031_1.fastq.gz	Fastqsanger.gz
	SRR8655031_2.fastq.gz	Fastqsanger.gz
	SRR8655032_1.fastq.gz	Fastqsanger.gz

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Transcriptome-wide m6A Methylation Profiling of Wild Type and ALKBH5-/- Peritoneal Macrophages by m6A-seq

Project description:By performing m6A-seq analysis on the peritoneal macrophages that derived from ALKBH5-/- mice and littermate mice infected with or without vesicular stomatitis virus (VSV), we want to investigate whether ALKBH5 deficiency-mediated m6A RNA methylation contributes to the regulation of its target genes expression. m6A-seq analysis revealed enriched and specific m6A peaks on the transcript of ALKBH5-targeted gene, which were substantially increased in ALKBH5-deficient peritoneal macrophages than that in wild-type cells whatever infected with or without VSV. Meanwhile we didn’t observe up-regulation of m6A signal on VSV in ALKBH5-deficient cells; and also didn't find significant difference of m6A signals on IFN-β mRNA between ALKBH5-deficient and wild type cells whatever infected with or without VSV. These demonstrated that deficiency of ALKBH5 controls viral replication by increasing the m6A modification of ALKBH5 target gene to regulate its expression.

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Next Generation Sequencing Analysis of the Transcriptomes of Wild Type and ALKBH5-/- Peritoneal Macrophages

Project description:By performing RNA sequencing (RNA-seq) analysis on the peritoneal macrophages that derived from ALKBH5-/- mice and littermate mice infected with or without vesicular stomatitis virus (VSV), we want to investigate whether deficiency of ALKBH5 controls viral replication through a more general mechanism such as enhancing innate response, and if not, what's the critical downstream target(s) of ALKBH5. RNA-seq analysis showed that mRNA expression of innate genes remained unchanged or not increased in ALKBH5-deficient cells. While thourgh KEGG pathway enrichment analysis of the RNA-seq data, we found that metabolic pathways were the ones most significantly affected in ALKBH5-deficient macrophages upon VSV infection. These results demonstrated that deficiency of ALKBH5 controls viral replication by significantly changing the metabolism-related genes expression.

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ALKBH5 is a New Mammalian RNA Demethylase

Project description:N6-methyladenosine (m6A) is the most prevalent internal modification of messenger RNA (mRNA) in higher eukaryotes. Here we report ALKBH5 as a new mammalian demethylase that oxidatively removes the m6A modification in mRNA in vitro and inside cells. This demethylation activity of ALKBH5 significantly affects mRNA export and RNA metabolism as well as the assembly of mRNA processing factors in nuclear speckles. Alkbh5-deficient male mice are characterized by impaired fertility resulting from apoptosis that affects meiotic metaphase-stage spermatocytes. In accordance with this defect, we have identified in mouse testes 1552 differentially expressed genes which cover broad functional categories and include spermatogenesis-related mRNAs involved in the p53 functional interaction network. We show that Alkbh5-deficiency impacts the expression levels of some of these mRNAs, supporting the observed phenotype. The discovery of this new RNA demethylase strongly suggests that the reversible m6A modification plays fundamental and broad functions in mammalian cells. RNA-seq in two cell types

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Project description:ALKBH5 is the RNA N(6)-methyladenosine (m6A) demethylase. To under sthand the function and mechnism of ALKBH5 in human acute myeloid leukemia, we compared the m6A profiling in wild-type, ALKBH5-knock-down, and ALKBH5 rescue THP1 cells.

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Project description:We performed the transcripome-wild m6A-sequencing to compare the m6A profiles of negative control (NC) HeLa cells and ALKBH5 KO HeLa cells stably re-expressing wild type ALKBH5 (WT) or its mutant K235R (K235R)

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ALKBH5 cooperated with LINC00659 promote gastric cancer progression by JAK1 mRNA m6A-YTHDF2-dependent modification [2-m6A]

Project description:N6-methyladenosine (m6A) modification is the most prevalent RNA epigenetic regulation in eukaryotic cells. Recent studies focused on the association between m6A and non-coding RNAs. The demethylase ALKBH5 acts as critical oncogenes or tumor suppressors through multiple mechanisms in various cancers. Here, we find that ALKBH5 is highly expressed in GC tissues and is associated with poor prognosis. ALKBH5 promoted the proliferation and metastasis both in vitro and in vivo. ALKBH5 was recruited by LINC00659, which removed m6A modifications of JAK1, leading to the upregulated expression of JAK1.Since ALKBH5 and LINC00659 have oncogenic role in gastric cancer (GC) progression with poor prognosis, ALKBH5-LINC00659/m6A/JAK1 axis can be new biological mechanisms behind GC development and future therapeutic opportunities.

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Chromatin state maintains human myeloid leukemia by regulating m6A demethylase ALKBH5 expression [RNA-Seq]

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