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Zebrafish preserve preserve germline epigenetic memory globally but demethylate and amplify sex-linked rDNA during feminisation

ABSTRACT: Zebrafish preserve preserve germline epigenetic memory globally but demethylate and amplify sex-linked rDNA during feminisation

PROVIDER: PRJNA506038 | ENA |

REPOSITORIES: ENA

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Zebrafish preserve preserve germline epigenetic memory globally but demethylate and amplify sex-linked rDNA during feminisation

Project description:The germline is unique because it is the only cellular lineage capable of transferring genetic information from one generation to the next. Intergenerational transmission of epigenetic memory is also possible; however, in mammals this is largely prevented by extensive epigenetic erasure during germline definition from somatic precursors. We report that the ‘preformed’ germline of zebrafish, defined by inheritance of cellular components from the egg and not cellular reprogramming, shows consistently high levels of DNA methylation throughout development. This demonstrates epigenetic erasure is not a barrier to transgenerational epigenetic inheritance in zebrafish and likely other vertebrates with preformed germlines. Our analysis also uncovered female-specific germline amplification and demethylation of an 11.5-kb repeat region encoding 45S ribosomal RNA (fem-rDNA). The peak of fem-rDNA expansion coincided with the initial expansion of stage IB oocytes, the poly-nucleolar cell type responsible for zebrafish feminisation. Given that fem-rDNA overlaps with the only zebrafish locus identified thus far as sex-linked, we hypothesize fem-rDNA expansion is intrinsic to sex determination in this species.

2018-11-20 | GSE122695 | GEO

Zebrafish preserve global germline DNA methylation while sex-linked rDNA is amplified and demethylated during feminisation.

Project description: Not available

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Oncogenic extrachromosomal DNA functions as mobile enhancers to globally amplify chromosomal transcription

Project description:Extrachromosomal, circular DNA (ecDNA) is emerging as a prevalent yet less characterized oncogenic alteration in cancer genomes. We leverage ChIA-PET and ChIA-Drop chromatin interaction assays to characterize genome-wide ecDNA-mediated chromatin contacts that impact transcriptional programs in cancers. ecDNAs in glioblastoma patient-derived neurosphere and prostate cancer cell cultures are marked by widespread intra-ecDNA and genome-wide chromosomal interactions. ecDNA-chromatin contact foci are characterized by broad and high-level H3K27ac signals converging predominantly on chromosomal genes of increased expression levels. Prostate cancer cells harboring synthetic ecDNA circles composed of characterized enhancers result in the genome-wide activation of chromosomal gene transcription. Deciphering the chromosomal targets of ecDNAs at single-molecule resolution reveals an association with actively expressed oncogenes spatially clustered within ecDNA-directed interaction networks. Our results suggest that ecDNA can function as mobile transcriptional enhancers to promote tumor progression and manifest a potential synthetic aneuploidy mechanism of transcription control in cancer.

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