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| Status |
Public on Jul 17, 2023 |
| Title |
Dot1l cooperates with Npm1 to repress endogenous retrovirus MERVL in embryonic stem cells |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
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| Summary |
Dot1l is a histone methyltransferase without a SET domain and is responsible for H3K79 methylation, which marks active transcription. In contradiction, Dot1l also participates in silencing gene expression. The target regions and mechanism of Dot1l in repressing transcription remain enigmatic. Here, we examined the possibility for Dot1l as an repressor of MERVL, which is a marker of 2-cell-like cells. Mechanistically, Dot1l interacted with and colocalized with Npm1 on MERVL, and depletion of Npm1 similarly augmented MERVL expression.
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| Overall design |
We knocked out Dot1l in E14 by CRISPR/Cas9 System. We performed RNA-seq analysis in order to exam the transcriptome after Dot1l KO, performed ChIP-seq analysis in order to exam the DNA binding sites of DOT1L and NPM1.
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| Citation(s) |
37522386 |
| |
| Submission date |
Apr 29, 2022 |
| Last update date |
Sep 27, 2023 |
| Contact name |
Haiyang Sun |
| Organization name |
Nankai University
|
| Street address |
No.38 Tongyan Road, Jinnan District
|
| City |
Tianjin |
| ZIP/Postal code |
300350 |
| Country |
China |
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| Platforms (1) |
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| Samples (10)
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| This SuperSeries is composed of the following SubSeries: |
| GSE201847 |
RNA-seq analysis about Dot1l knocked out samples |
| GSE201848 |
ChIP-seq analysis about Dot1l and Npm1 samples |
|
| Relations |
| BioProject |
PRJNA833294 |
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