Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA229454 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1035220.fastq.gz | Fastqsanger.gz | |||
| SRR1035221.fastq.gz | Fastqsanger.gz | |||
| SRR1035222.fastq.gz | Fastqsanger.gz | |||
| SRR1035213.fastq.gz | Fastqsanger.gz | |||
| SRR1035223.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:m6A RNA modification controls cell fate transition in mammalian embryonic stem cells (RNA methylation)
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Project description:m6A RNA modification controls cell fate transition in mouse embryonic stem cells
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Project description:m6A RNA modification controls cell fate transition in mouse embryonic stem cells (gene expression analysis)
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Project description:N6-methyl-adenosine (m6A) is the most abundant modification on messenger RNAs and is linked to human diseases, but its functions in mammalian development are poorly understood. Here we reveal the evolutionary conservation and function of m6A by mapping the m6A methylome in mouse and human embryonic stem cells. Thousands of messenger and long noncoding RNAs show conserved m6A modification, including transcripts encoding core pluripotency transcription factors. m6A is enriched over 3M-bM-^@M-^Y untranslated regions at defined sequence motifs, and marks unstable transcripts, including transcripts turned over upon differentiation. Genetic inactivation or depletion of mouse and human Mettl3, one of the m6A methylases, led to m6A erasure on select target genes, prolonged Nanog expression upon differentiation, and impaired ESCM-bM-^@M-^Ys exit from self-renewal towards differentiation into several lineages in vitro and in vivo. Thus, m6A is a mark of transcriptome flexibility required for stem cells to differentiate to specific lineages. Examing m6A modification differences in two different cell types
2014-10-20 | E-GEOD-52600 | 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:N6-methyladenosine (m6A) represents the most prevalent internal modification on messenger RNA, and requires a multicomponent m6A methyltransferase complex in mammals. How their plant counterparts determine the global m6A modification landscape and its molecular link to plant development remain elusive. Here we show that FKBP12 INTERACTING PROTEIN 37 KD (FIP37) is a core component of the m6A methyltransferase complex, which underlies control of shoot stem cell fate in Arabidopsis. The mutants lacking FIP37 exhibit massive overproliferation of shoot meristems and a transcriptome-wide loss of m6A RNA modifications. We further demonstrate that FIP37 mediates m6A RNA modification on key shoot meristem genes inversely correlated with their mRNA stability, thus confining their transcript levels to prevent shoot meristem overproliferation. Our results suggest an indispensable role of FIP37 in mediating m6A mRNA modification, which is required for maintaining the shoot meristem as a renewable source for continuously producing all aerial organs in plants. m6A-seq in Arabidopsis thaliana (Col-0) wild-type and fip37-4 LEC1:FIP37, two replicates for each sample
2016-07-25 | E-GEOD-75506 | biostudies-arrayexpress
Project description:N6-methyladenosine (m6A) represents the most prevalent internal modification on messenger RNA, and requires a multicomponent m6A methyltransferase complex in mammals. How their plant counterparts determine the global m6A modification landscape and its molecular link to plant development remain elusive. Here we show that FKBP12 INTERACTING PROTEIN 37 KD (FIP37) is a core component of the m6A methyltransferase complex, which underlies control of shoot stem cell fate in Arabidopsis. The mutants lacking FIP37 exhibit massive overproliferation of shoot meristems and a transcriptome-wide loss of m6A RNA modifications. We further demonstrate that FIP37 mediates m6A RNA modification on key shoot meristem genes inversely correlated with their mRNA stability, thus confining their transcript levels to prevent shoot meristem overproliferation. Our results suggest an indispensable role of FIP37 in mediating m6A mRNA modification, which is required for maintaining the shoot meristem as a renewable source for continuously producing all aerial organs in plants. RNA-seq in Arabidopsis thaliana (Col-0) wild-type and fip37-4 LEC1:FIP37, three replicates for each sample
2016-07-25 | E-GEOD-75507 | 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:N6-methyladenosine (m6A) is the most abundant and reversible modification on messenger RNAs. The differential m6A profiles in different cell types are installed by writers (such as METTL3) and removed by erasers (such as FTO). The m6A-modified RNAs are recognized by readers to trigger downstream regulation of RNA metabolism, eventually contributing to the regulation of cell fates. Primordial germ cells (PGCs) are specified early during embryogenesis and establish the germ cell lineage for transmitting genetic and epigenetic information from parents to offspring. Defects in the establishment of germline may lead to infertility, germ cell tumors, and birth defects. Despite extensive research, the m6A-mediated epigenetic regulation of the specification of PGCs remains elusive. In this study, we discovered that knock-out of m6A writer or over-expression of erasers leads to increased percentage of human PGC-like cells (hPGCLCs) induced from embryonic stem cells. We identified the m6A reader IGF2BP1 as the key factor for restricting hPGCLC fate induction by stabilizing OTX2 mRNAs in an m6A-dependent manner. Moreover, we discovered that OTX2 suppresses TFAP2C during germ cell lineage specification. In summary, we characterized the m6A-IGF2BP1-OTX2-TFAP2C axis in restricting the specification of human germ cell fate.
2024-04-30 | PXD051996 |
Project description:In this study we identify Mettl3, an m6A RNA modification writer, as a critical regulator for terminating naïve pluripotency and a positive maintainer of primed pluripotency in vitro and in vivo. Remarkably, Mettl3 knockout pre-implantation epiblasts and naïve ES cells, entirely lack m6A on coding mRNAs and are viable. Yet, they fail to adequately terminate the naïve pluripotent state, and subsequently undergo aberrant priming and early lineage commitment at the post-implantation stage. A comprehensive functional and genomic analysis involving profiling of m6A, RNA transcription and translation in Mettl3 wild-type and knockout pluripotent and differentiated cells, identified m6A as a critical determinant that destabilizes secondary naïve specific pluripotency genes Esrrb, Klf4 and Nanog, and restrains their transcript stability and translation efficiency. In summary, our findings provide for the first time evidence for a critical role for an mRNA epigenetic modification in early mammalian development in vivo, and identify a mechanism that functionally regulates mouse naïve and primed pluripotency in an opposing manner. Ribosome footprint (Ribo-Seq) was measured from mouse embryonic stem cells and mouse embriod bodies, in WT and Mettl3-KO cell lines.
2014-11-02 | E-GEOD-61996 | biostudies-arrayexpress