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Effect of depletion of ALKBH5 on transcriptional landscape in human neutrophils during bacterial infection

ABSTRACT: Effect of depletion of ALKBH5 on transcriptional landscape in human neutrophils during bacterial infection

PROVIDER: PRJNA934494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23352277_1.fastq.gz	Fastqsanger.gz
	SRR23352277_2.fastq.gz	Fastqsanger.gz
	SRR23352278_1.fastq.gz	Fastqsanger.gz
	SRR23352278_2.fastq.gz	Fastqsanger.gz
	SRR23352279_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of ALKBH5 on transcriptional landscape in human neutrophils during bacterial infection

Project description:By performing RNA-seq analysis on ALKBH5-deficient (ALKBH5-/-, KO) and Wild-type (WT) dHL-60 human neutrophils infected with Escherichia coli, we want to investigate the effect of ALKBH5 on transcriptional landscape of human neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.

2023-12-21 | GSE224650 | GEO

Effect of depletion of ALKBH5 on transcriptional landscape in bone marrow neutrophils from septic mice

Project description:By performing RNA-seq analysis on bone marrow neutrophils from the Alkbh5-deficient mice and Wild-type littermates undergoing CLP-induced sepsis, we want to investigate the effect of ALKBH5 on transcriptional landscape of mouse bone marrow neutrophils during bacterial infection. Then, we performed gene expression profiling and Gene Ontology enrichment analysis of the significantly differentially expressed genes using data obtained from RNA-seq.

2023-12-21 | GSE224651 | GEO

Next Generation Sequencing and Analysis of the Transcriptomes of Wild-type and Alkbh5-/- Neutrophils

Project description:By performing transcriptome-wide RNA sequencing (RNA-seq) analysis on the peritoneal neutrophils from Alkbh5-deficient mice (Alkbh5-/-) and Wild-type littermates (Alkbh5+/+) at 12h or 36h after mild cecal ligation and puncture (CLP), respectively, we want to identify potential targets of ALKBH5 and characterize the transcriptional landscape in neutrophils during antibacterial innate defense. Gene Ontology biological processes enrichment analysis of the significantly differentially expressed genes (DEGs) showed that neutrophil migration made up the most significantly enriched biological processes with annotations of neutrophil association upon loss of ALKBH5 in neutrophils, at both 12h and 36h after CLP. Many significantly DEGs also encompassed transcriptional signatures related to neutrophils, specifically to neutrophil influx into the infection site, including chemotaxis, response to chemokine, extravasation, ERK1 and ERK2 cascade, homeostasis of neutrophils. ALKBH5 deletion led to significantly decreased transcript expression of neutrophil migration-promoting Cxcr2 and Nlrp12; while increased transcript expression of neutrophil migration-suppressive Ptger4, Tnc, and Wnk1. These results demonstrated that ALKBH5 imprints migration-promoting transcriptional landscape in neutrophils to enable their migration into the site of infection for antibacterial innate defense.

2022-05-24 | GSE198316 | GEO

Effect of depletion of ALKBH5 on transcriptional landscape in bone marrow neutrophils from septic mice

Project description:Effect of depletion of ALKBH5 on transcriptional landscape in bone marrow neutrophils from septic mice

| PRJNA934493 | ENA

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

2013-02-15 | E-GEOD-40132 | biostudies-arrayexpress

ALKBH5

Project description:ALKBH5

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Effect of depletion of ALKBH5 on gene expression of HaCAT human keratinocyte cell line

Project description:To investigate the function of ALKBH5 in the regulation of keratinocyte cellular function, we established HaCAT cell lines in which ALKBH5 has been knocked down by siRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells from duplicate experiments.

2022-08-12 | GSE211076 | GEO

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

Project description:N6-methyladenonsine (m6A) modification locates ubiquitously in mammalian mRNA, and profoundly impacts various physiological processes and pathogenesis. However, the precise involvement of m6A in early endoderm development has yet to be fully elucidated. Here, we reported that depletion of the m6A demethylase ALKBH5 in human embryonic stem cells (hESCs) severely impaired definitive endoderm (DE) differentiation. Within this process, ALKBH5-/- hESCs failed to undergo the primitive streak (PS) intermediate transition, which is considered as a prelude to endoderm specification. Mechanistically, we demonstrated that ALKBH5 deficiency induced m6A hypermethylation around the 3’ untranslated region (3’UTR) of GATA6 transcripts and destabilized GATA6 mRNA in a YTHDF2-dependent manner. Moreover, dysregulation of GATA6 expression ablated its occupancy with critical regulators of Wnt/β-catenin signaling pathway, thereby disrupting the signaling logic underlying DE formation. Overall, our findings unveil a mechanism whereby the ALKBH5-GATA6-WNT/β-catenin axis modulates human in vitro DE induction, and present novel insights on m6A modification in early embryonic development.

2024-10-23 | GSE248527 | GEO