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Nanopore sequencing reveals the roles of spermatozoal DNA N6-Methyladenine modification in mediating transgenerational lipid metabolism disorder induced by folic acid excessive consumption in chicken [RNA-seq]

ABSTRACT: Nanopore sequencing reveals the roles of spermatozoal DNA N6-Methyladenine modification in mediating transgenerational lipid metabolism disorder induced by folic acid excessive consumption in chicken [RNA-seq]

PROVIDER: PRJNA685411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13255573_1.fastq.gz	Fastqsanger.gz
	SRR13255573_2.fastq.gz	Fastqsanger.gz
	SRR13255574_1.fastq.gz	Fastqsanger.gz
	SRR13255574_2.fastq.gz	Fastqsanger.gz
	SRR13255575_1.fastq.gz	Fastqsanger.gz

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Nanopore sequencing reveals the roles of spermatozoal DNA N6-Methyladenine modification in mediating transgenerational lipid metabolism disorder induced by folic acid excessive consumption in chicken [RNA-seq]

Project description:Increased consumption of folic acid is prevalent due to its beneficial effects to help protecting from genome damage. Growing evidence is emphasizing the side effects pointing to excessive dietary intake. Effects of paternal folic acid excessive consumption on the offspring and its transgenerational inheritance mechanism remain elusive. We hypothesize that the folic acid excessive consumption will alter sperm DNA N6-methyladenine (6mA) and 5-methylcytosine (5mC) methylation, and heritably influence offspring metabolic homeostasis. This is the results of mRNA sequencing part

2020-12-16 | GSE163238 | GEO

Nanopore sequencing demonstrates the roles of spermatozoal DNA N6-methyladenine in mediating transgenerational lipid metabolism disorder induced by excessive folate consumpton.

Project description:Increased consumption of folic acid is prevalent due to its beneficial effects, but growing evidence emphasizes the side effects pointing to excessive dietary folate intake. The effects of excessive paternal folic acid consumption on offspring and its transgenerational inheritance mechanism have not been elucidated. We hypothesize that excessive folic acid consumption will alter sperm DNA N6-methyladenine (6mA) and 5-methylcytosine (5mC) methylation and heritably influence offspring metabolic homeostasis. Here, we fed roosters either folic acid-control or folic acid-excess diet throughout life. Paternal chronic folic acid excessive supplementation increased hepatic lipogenesis and lipid accumulation but reduced lipolysis both in the roosters and their offspring, which was further confirmed to be induced by one-carbon metabolism inhibition and gene expression alteration associated with the Peroxisome proliferator-activated receptor pathway. Based on the spermatozoal genome-wide DNA methylome identified by Nanopore sequencing, multi-omics association analysis of spermatozoal and hepatic DNA methylome, transcriptome, and metabolome suggested that differential spermatozoal DNA 6mA and 5mC methylation could be involved in regulating lipid metabolism-related gene expression in offspring chickens. This model suggests that sperm DNA N6-methyladenine and 5-methylcytosine methylation were involved in epigenetic transmission and that paternal dietary excess folic acid leads to hepatic lipid accumulation in offspring.

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Project description:Nanopore sequencing reveals the roles of spermatozoal DNA N6-Methyladenine modification in mediating transgenerational lipid metabolism disorder induced by folic acid excessive consumption in chicken

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