RNA sequencing of spermatogonia with different m6a methylation
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ABSTRACT:
PROVIDER: PRJNA750056 | ENA |
REPOSITORIES: ENA
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Project description:we knocked down the expression level of METTL3 in spermatogonia to reduce the total m6A methylation in the cells, and mapped the RNA expression profile of spermatogonia after the total m6A methylation level was reduced，and we after the m6A methylation was reduced, many lncRNA and mRNA were differently expressed
2023-08-15 | GSE180909 | GEO
Project description:we knocked down the expression level of METTL3 in spermatogonia to reduce the total m6A methylation in the cells, and mapped the small RNA expression profile of spermatogonia after the total m6A methylation level was reduced，and we after the m6A methylation was reduced, many miRNA and circRNA were differently expressed
2023-08-15 | GSE201965 | GEO
Project description:small RNA sequencing of spermatogonia with different m6a methylation
| PRJNA833869 | ENA
Project description:XIST is a long non-coding RNA (lncRNA) that mediates transcriptional silencing of X chromosome genes. Here we show that XIST is highly methylated with at least 78 N6-methyladenosine (m6A) residues, a reversible base modification whose function in lncRNAs is unknown. We show that m6A formation in XIST, as well as cellular mRNAs, is mediated by RBM15 and its paralog RBM15B, which bind the m6A-methylation complex and recruit it to specific sites in RNA. This results in methylation of adenosines in adjacent m6A consensus motifs. Furthermore, knockdown of RBM15 and RBM15B, or knockdown of the m6A methyltransferase METTL3 impairs XIST-mediated gene silencing. A systematic comparison of m6A-binding proteins shows that YTHDC1 preferentially recognizes m6A in XIST and is required for XIST function. Additionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m6A. These data reveal a pathway of m6A formation and recognition required for XIST-mediated transcriptional repression. Three to four biological HEK293T replicates were used to perform iCLIP of endogenous YTH proteins, RBM15, and RBM15B. Crosslinking induced truncations were identified using CIMS-CITS pipeline.
2016-09-07 | E-GEOD-78030 | biostudies-arrayexpress
Project description:Here we determine the map of RNA methylation (m6A) in mouse embrionic stem cells, and Mettl3 knock out cells Examination of m6A modification sites on the transcriptome of mouse Embryonic stem cells and Embryonic Mettl3 knock out cells, using a m6A specific antibody.
2014-10-16 | E-GEOD-52662 | biostudies-arrayexpress
Project description:Spermatogenesis, an efficient and complex system in male germline development, requires a series of elaborately regulated genetic events in which diploid spermatogonia differentiate into haploid spermatozoa. N6-methyladenosine (m6A) is important for spermatogenesis. ALKBH5 is an m6A eraser, and knockout of ALKBH5 increases the level of total m6A methylation and causes male infertility.
2021-12-13 | GSE186217 | GEO
Project description:Human neurodevelopment requires differentiating neurons to establish large networks of connections in a highly stereotyped manner. Neuronal differentiation in particular, requires RNA-binding proteins to spatiotemporally regulate thousands of different mRNAs. Yet, how these proteins precisely relate to neuronal development and coordinate the expression of functionally coherent genes in a cell type specific manner is only partially understood. To address this, we sought to understand how the paradigmatic RNA-binding protein IMP1/IGF2BP1, an essential developmental factor, selects and regulates its RNA targets transcriptome-wide during the differentiation of human neurons. We used a combination of systemic and molecular analyses to show that IMP1 directly binds to and regulates the expression of a large set of mRNAs that govern microtubule assembly, an essential process and a key driver of neuronal differentiation. We also show that m6A methylation during the transition from neural precursors to neurons drives both the selection of IMP1 mRNA targets and their translation potential. Our findings establish m6A methylation as a key mechanism coordinating the regulatory action of IMP1 on human neuronal architecture.
2024-06-10 | PXD034341 | Pride
Project description:m6A is a ubiquitous RNA modification in eukaryotes. Transcriptome-wide m6A patterns in Arabidopsis have been assayed recently. However, m6A differential patterns among organs have not been well characterized. The goal of the study is to comprehensively analyze m6A patterns of numerous types of RNAs, the relationship between transcript level and m6A methylation extent, and m6A differential patterns among organs in Arabidopsis. In total, 18 libraries were sequneced. For the 3 organs: leaf, flower and root, each organ has mRNA-Seq, m6A-Seq and Input sequenced. And each sequence has 2 replicats.
2015-10-28 | E-GEOD-72706 | biostudies-arrayexpress
Project description:N6-methyladenosine (m6A) has been recently identified as a conserved epitranscriptomic modification of eukaryotic mRNAs, but its features, regulatory mechanisms, and functions in cell reprogramming are largely unknown. Here, we report m6A modification profiles in the mRNA transcriptomes of four cell types with different degrees of pluripotency. Comparative analysis reveals several features of m6A, especially gene- and cell-type-specific m6A mRNA modifications. We also show that microRNAs (miRNAs) regulate m6A modification via a sequence pairing mechanism. Manipulation of miRNA expression or sequences alters m6A modification levels through modulating the binding of METTL3 methyltransferase to mRNAs containing miRNA targeting sites. Increased m6A abundance promotes the reprogramming of mouse embryonic fibroblasts (MEFs) to pluripotent stem cells; conversely, reduced m6A levels impede reprogramming. Our results therefore uncover a role for miRNAs in regulating m6A formation of mRNAs and provide a foundation for future functional studies of m6A modification in cell reprogramming. m6A-seq in ESC, iPSC, NSC and sertoli cells.
2015-03-10 | E-GEOD-52125 | biostudies-arrayexpress
Project description:In this study, we identified METTL16 as an mRNA m6A methyltransferase that plays a vital role in the floral transition in Arabidopsis. Transcriptome-wide analysis of RNA methylome in the mettl16 mutant revealed that m6A modification enriched near the stop codon and within the 3ʹ untranslated region. Deficiency of METTL16 leads to decreases in m6A levels of approximately 471 transcripts, indicating that it is responsible for the methylation of a small group of mRNAs. The mettl16 mutant displayed an early flowering phenotype, and the level of FLOWERING LOCUS C (FLC) was markedly decreased in the mutant. Importantly, METTL16-mediated m6A methylation affects the splicing of FLC, thereby influencing its transcript level to regulate floral transition. Our study identified METTL16 as a novel m6A methyltransferase and suggests a close molecular link between METTL16-mediated m6A methylation and FLC splicing in flowering time control.
2021-08-07 | GSE180768 | GEO