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AMPKα2 knockout mice and usage of alternative transcription start sites

ABSTRACT: AMPKα2 knockout mice and usage of alternative transcription start sites

PROVIDER: PRJNA445690 | ENA |

REPOSITORIES: ENA

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AMPKα2 knockout mice and usage of alternative transcription start sites

Project description:Role of alternative transcription start sites in muscle growth and development remains largely undetermined. Our WTSS-seq (whole transcriptome start site sequencing) approach to capture 5'-end of RNAs clearly revealed alternative transcription start events responsible for increased muscle mass in AMPK α2 knockout mice.

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AMPKα1 and α2 knockout and usage of alternative polyadenylation sites

Project description:AMPKα1 and α2 knockout and usage of alternative polyadenylation sites

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Profiling of alternative transcription start sites and alternative polyadenylation sites in Xenopus tropicalis

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BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

Project description:Pervasive usage of alternative promoters leads to deregulation of gene expression in carcinogenesis and may drive the emergence of new genes in spermatogenesis. However, little is known regarding the mechanisms underpinning the activation of alternative promoters. In our present study, we uncovered a novel mechanism by which alternative cancer-testis-specific transcription is activated from the intergenic and intronic clustered CTCF binding sites, which are transcriptionally inert in normal somatic cells. BORIS/CTCFL, a paralog of CTCF with cancer-testis-specific expression forms a heterodimer with CTCF at the clustered binding sites thus triggering epigenetic reprogramming of these sites into units of active transcription. BORIS binding to CTCF sites leads to the recruitment of chromatin-remodeling factor SRCAP, with subsequent replacement of H2A histone with H2A.Z, therefore creating a more relaxed chromatin state in the nucleosomes flanking the clustered binding sites. This facilitates opening of chromatin beyond CTCF/BORIS binding sites and paves the way to the recruitment of multiple additional transcription factors, thereby activating transcription from a given binding site. We demonstrate that the CTCF binding sites, epigenetically reprogrammed by ectopic BORIS expression can drive the expression of cancer-testis genes, long-noncoding RNAs, retro-pseudogenes, and dormant transposable elements harbored by activated long transcripts. Taking together, our results reveal that BORIS functions as a transcription factor that epigenetically reprograms clustered CTCF binding sites into transcriptional start sites, promoting transcription from alternative promoters in both germ cells and cancer cells.

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AMPKα1 and α2 knockout and usage of alternative polyadenylation sites

Project description:Role of alternative polyadenylation in muscle development remains largely undetermined. Our WTTS-seq approach to capture 3'-end of RNAs clearly revealed alternaitve polyadenylation events responsible for reduced muscle mass in AMPK α1, but increased muscle mass in AMPK α2 knockout mice.

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Precise mapping of the transcription start sites of human microRNAs using DROSHA knockout cells

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