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Helicobacter pylori infection aggravates hepatic steatosis by lactylation-driven WTAP-mediated m6A modification

ABSTRACT: Helicobacter pylori (H. pylori) infection has been investigated as a potential risk factor for extragastric diseases, including metabolic dysfunction-associated fatty liver disease (MASLD). However, the details of the underlying mechanisms remain inadequately understood. In this study, we elucidate that H. pylori infection exacerbates hepatic metabolic disorders both in vitro and in vivo, manifesting as increased lipid deposition and insulin resistance. Mechanistically, H. pylori infection further upregulates m6A content, particularly increasing the expression of one of the m6A methyltransferases, WTAP.

ORGANISM(S): Homo sapiens

PROVIDER: GSE301711 | GEO | 2025/12/30

REPOSITORIES: GEO

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TTC22 increasing total m6A RNA level and colon cancer metastasis via RPL4-WTAP-YTHDF1 axis

Project description:WTAP is an essential component of the RNA N-6-methyladenosine (m6A) modification complexes that guides METLL3-METLL14 heteroduplexes to target RNAs in the nucleus of mammalian cells. Through mining the genotype-tissue expression (GTEx) datasets, we initially found that TTC22 expression was highly correlated with WTAP and FTO in many normal human tissues. Our experimental results indicate that TTC22 could directly capture RNA binding protein RPL4, induce the binding between RPL4 and WTAP mRNA in the cytoplasm, which increased the m6A level, induced alterative splicing, enhanced the stability and translation efficiency of WTAP mRNA, and consequently upregulated the level of total m6A RNA. These results indicate that WTAP mRNA is a m6A target and there is a positive feedback loop between total m6A and WTAP expression. YTHDF1 was found to be an essential m6A WTAP mRNA binding protein. Downregulation of RPL4, WTAP, or YTHDF1 expression could reverse TTC22-enhanced total m6A RNA level. m6A-specific antibody immunoprecipitated RNA-sequencing (meRIP-seq) demonstrated that TTC22 caused dramatic expression changes of genes related to metabolic pathways, ribosome biogenesis, and RNA spliceosome. Furthermore, we also found that TTC22 upregulated the expression of epithelial-mesenchymal transition (EMT)-related gene SNAI1 via m6A, and promoted metastasis of colon cancer in vitro and in mice. In conclusion, our study illustrates that WTAP mRNA is a m6A target using YTHDF1 as the binding protein. TTC22 could upregulate the levels of WTAP expression and total m6A RNA through the PRL4 binding. The m6A-mediated upregulation of SNAI1 expression may contribute to TTC22-enhanced colon cancer metastasis.

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Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL3, METTL14 and WTAP are the components of m6A methyltransferase complex. To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 and METTL3, METTL14 or WTAP knockdown HepG2 cells, and found depletion of H3K36me3 by SETD2 silencing globally reduced m6A in human transcriptome. What’s more, most of the SETD2-dependent hypomethylation sites also responded to knockdown of METTL3, METTL14, or WTAP.

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The effects of WTAP on m6A mRNA modification pancreatic islets

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ZC3H13 and WTAP KO in hMDMs multi stimuli(NGS5421)

Project description:Here, we revealed an immunosuppressive role of m6A mediated by ZC3H13 and WTAP on TNF-driven inflammatory phenotype in human macrophages. In the following experiment we would like to investigate if the negative regulatory role of m6A is consistent across multiple stimuli using innate ligands (LPS, R848 and polyIC). We generated ZC3H13 KOs, WTAP KOs and NTC (WT) in monocyte-derived macrophages from 4 individual human donors and stimulated cells over night with LPS (5ng/ml) , R848 (50ng/ml) , polyIC (50ng/ml) and unstimulated cells as control. This yielded a total of 48 total samples.

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Project description:Purpose: Through mRNA m6A-profiling, we aim to characterize the mRNA m6A changes in the liver obtained from Wtapflox/flox and Wtap-HKO mice. Methods: Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany) from liver of Wtap flox/flox and Wtap-HKO mice at 8 weeks old. Each sample (300 μg total RNA) was pooled from 5 mice for each group. Two independent biological replicates for each group were used for m6ARIP-seq. Poly(A)+ RNA was purified using Dynabeads™ mRNA Purification Kit (Invitrogen) following the manufacturer’s instructions. Fragmented mRNA was incubated with m6A antibody (Synaptic System, 202003) for immunoprecipitation. Then, immunoprecipitated mRNAs or Input was used for library construction with NEBNext ultra RNA library prepare kit for Illumina (New England Biolabs).The library preparations were sequenced on an Illumina Novaseq 6000 platform with a paired-end read length of 150 bp according to the standard protocols. The m6A peaks were detected by exomePeak R package (version 2.16.0). The motif search was detected by HOMER(version 4.9.1). Conclusion: The mRNA m6A profiles in the liver of Wtapflox/flox and Wtap-HKO mice were characterized.

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2014-01-16 | E-GEOD-50580 | biostudies-arrayexpress

LOX-1 is an N6-methyladenosine-regulated receptor for Helicobacter pylori via binding to the bacterial catalase [m6A-seq]

Project description:The role of N6-methyladenosine (m6A) modification of host mRNA during bacterial infection is unclear. Here, we show that Helicobacter pylori infection upregulated major m6A “writers” and increased m6A level in gastric epithelial cells. Attenuating m6A increase by hemizygotic deletion of Mettl3 in mice or small interfering RNAs targeting m6A “writers” exacerbated H. pylori colonization. LOX-1 mRNA was identified as a key m6A-regulated target during H. pylori infection. m6A modification destabilized LOX-1 mRNA and reduced LOX-1 protein level. LOX-1 acted as a membrane receptor for H. pylori catalase to mediate the bacterial adhesion. BI-0115, a small-molecule inhibitor of LOX-1, suppressed H. pylori adhesion and colonization. Genetic ablation of Lox-1 also reduced H. pylori colonization in mice. In sum, this study reveals that m6A modification is an auto-protective mechanism against H. pylori infection by downregulating LOX-1 to prevent H. pylori adhesion. LOX-1 could be a druggable target for controlling H. pylori infection.

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