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MeDIP-seq profile of Sam-S overexpressed female Drosophila germline.

ABSTRACT: MeDIP-seq profile of Sam-S overexpressed female Drosophila germline.

PROVIDER: PRJNA1248517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33048055.fastq.gz	Fastqsanger.gz
	SRR33048056.fastq.gz	Fastqsanger.gz
	SRR33048057.fastq.gz	Fastqsanger.gz
	SRR33048058.fastq.gz	Fastqsanger.gz
	SRR33048059.fastq.gz	Fastqsanger.gz

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MeDIP-seq profile of Sam-S overexpressed female Drosophila germline.

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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