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Chromatin and gene expression changes during female Drosophila germline stem cell development.

ABSTRACT: Chromatin and gene expression changes during female Drosophila germline stem cell development.

PROVIDER: PRJNA956868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24203628.fastq.gz	Fastqsanger.gz
	SRR24203629.fastq.gz	Fastqsanger.gz
	SRR24203630.fastq.gz	Fastqsanger.gz
	SRR24203631.fastq.gz	Fastqsanger.gz
	SRR24203632.fastq.gz	Fastqsanger.gz

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Chromatin and gene expression changes during female Drosophila germline stem cell development.

Project description:The maintenance and differentiation of highly potent animal stem cells generates an epigenetic cycle that underlies development. Drosophila female germline stem cells (GSC) produce cystoblast daughters that differentiate into nurse cells and oocytes. Developmental chromatin analysis profiling the differentiation of GSCs into cystoblasts and NCs of increasing ploidy shows that cystoblasts start developing by forming heterochromatin while in a transient syncytial state, the germline cyst, reminiscent of early embryonic cells. The open GSC chromatin state is further restricted by Polycomb repression of targets that include testis expressed genes briefly active in early female germ cells. Like other highly potent stem cells, GSC metabolism is reprogrammed and Myc-dependent growth is upregulated by altering mitochondrial membrane transport, gluconeogenesis and other processes. Thus, the animal generational cycle comprises similar but distinct maternal and zygotic stem cell epigenetic cycles. We propose that the pluripotent stem cell state and daughter cell differentiation were shaped by the pressure to resist transposon activity over evolutionary time scales. In this GEO submission, we present data and analyses pertaining to H3K27ac, H3K27me3, and H3K9me3 ChIPseq, ATACseq, and RNAseq of Germline Stem Cells (GSCs) and Nurse Cells (NCs) from Drosophila melanogaster ovaries.

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Project description:The gene-regulatory mechanisms behind the female germline piRNA pathway in ovaries of metazoan species remain largely unexplored. Here, using the Drosophila model and combinations of RNA-seq, ATAC-seq, and single-cell approaches, we reveal the transcription factors that regulate the female germline piRNA pathway in animal ovaries.

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Project description:The gene-regulatory mechanisms behind the female germline piRNA pathway in ovaries of metazoan species remain largely unexplored. Here, using the Drosophila model and combinations of ChIP-seq, RNA-seq, ATAC-seq, and single-cell approaches, we reveal the transcription factors that regulate the female germline piRNA pathway in animal ovaries.

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Project description:S-adenosylmethionine (SAM) is the principal cellular donor of methyl-moiety in methylation reaction and regulates gene expression by regulating methylation related cellular events, such as epigenetic regulation. Although SAM biosynthesis affects variety of biological phenomena including disease and aging, whether cell-specific SAM biosynthesis status present and how it contributes cellular function are largely unknow. Here, we firstly showed that Drosophila germline in gametogenesis has repressive SAM biosynthesis status through observation of SAM synthetase (Sam-S), a key enzyme for SAM biosynthesis. In addition, our study showed that germline-unique repressive SAM biosynthesis status contributes to inhibition of retrotransposon expression; enhancement of SAM biosynthesis in germline caused excessive expression of retrotransposons including HeT-A, a telomere-specific retroelement, as the most affected target. We found that promoter activity of HeT-A is enhanced in SAM increased condition with increased accumulation of 6mA DNA methylation, the major DNA methylation modification in Drosophila genome. Interestingly, the enhanced 6mA enrichment and gene expression in enriched loci was not correlated in neither other retrotransposons nor structural genes. Taken together, our results suggest SAM-deficient status in germline uniquely regulates HeT-A transcription via 6mA methylation modification. Thus, our study provides new understanding how germline unique metabolic status contributes to regulation of retrotransposon expression.

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