Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To understand the role of YTHDF2 in AML, we generated m6A meRIP-seq libraries form Ythdf2fl/fl (Ythdf2CTL) pre-leukemic cells.
Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To understand the role of YTHDF2 in AML, we generated m6A meRIP-seq libraries form Ythdf2fl/fl; Vav-iCre (Ythdf2CKO) pre-leukemic cells.
Project description:Background: Abdominal aortic aneurysm (AAA) is a vascular disease with indeterminate prevalence but high mortality rates when complicated with rupture. The pathogenesis of AAA has not been fully elucidated. N6-methyladenosine (m6A) modification is likely important in the development of AAA. In the present study, m6A-MeRIP sequencing and RNA sequencing were performed to identify the m6A sites. Bioinformatics analysis was used to evaluate the m6A patterns of the aorta walls of AngII-induced abdominal aortic aneurysm (AAA) model and normal mice. Results: There were 2039 differentially methylated m6A peaks involving 1865 mRNAs in the AAA group relative to the control, of which 1610 peaks in 1466 mRNAs were hypermethylated and 429 peaks in 410 mRNAs were hypomethylated. The hypermethylated mRNAs in AAA group were mostly enriched in transcription regulation and intercellular signaling, especially the Wnt signaling-associated processes. Hypomethylated m6A sites were mainly enriched in G protein-coupled receptor activity and ion channel activity. Conclusion: Our study suggested an original viewpoint that AAA might mainly be relevant to combined effect of m6A methylation modification in Wnt pathway, G protein-coupled receptor and ion channel- associated genes, which were worthy of further investigation.
Project description:Total RNAs were isolated from WT splenic NK cells, and subjected to standard m6A MeRIP, in two replicates, using Illumina Novaseq 6000 platform. The raw sequencing reads were mapped to the genome of Mus musculus (mm10) with default parameters. ExomePeak was used to identify m6A peaks, which were annotated by intersection with gene architecture using ChIPseeker. Sequence motifs enriched in peak regions were identified using Homer.
Project description:Many transcriptional and epigenetic networks must be integrated to maintain self-renewal and pluripotency in embryonic stem cells (ESCs) and to enable induced pluripotent stem cell (iPSC) reprogramming. Here, we explore the role of Zfp217 as a key transcriptional factor in maintaining ES cell self-renewal by performing meRIP analysis in control and Zfp217-depleted mouse stem cells. Examination of m6A levels from total RNA in control and Zfp217 shRNA infected mouse stem cells
Project description:To assess the m6A methylome during denervation-induced muscle atrophy, the methylated RNA immunoprecipitation sequencing (MeRIP-seq) was performed.
Project description:In this study, we aimed to systematically profile global RNA N6-methyladenosine (m6A) modification patterns in a mouse model of diabetic cardiomyopathy (DCM). Patterns of m6A in DCM and normal hearts were analyzed via m6A-specific methylated RNA immunoprecipitation followed by high-throughput sequencing (MeRIP-seq) and RNA sequencing (RNA-seq). A total of 973 m6A peaks were detected in DCM samples and 296 differentially methylated sites were selected for further study, including 106 hypermethylated and 190 hypomethylated m6A sites (fold change (FC) > 2, p < 0.05). Gene ontology and KEGG Pathway analyses indicated that unique m6A-modified transcripts in DCM were closely linked to cardiac fibrosis, myocardial hypertrophy, and myocardial energy metabolism. Overall, m6A modification patterns were altered in DCM, and modification of epitranscriptomic processes, such as m6A, is a potentially interesting therapeutic approach.