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Caenorhabditis elegans

ABSTRACT: Transgenerational inheritance of mitochondrial stress adaptation in C. elegans

PROVIDER: PRJNA339523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4044260_1.fastq.gz	Fastqsanger.gz
	SRR4044260_2.fastq.gz	Fastqsanger.gz
	SRR4044261_1.fastq.gz	Fastqsanger.gz
	SRR4044261_2.fastq.gz	Fastqsanger.gz
	SRR4044262_1.fastq.gz	Fastqsanger.gz

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Transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans

Project description:Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents.

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Project description:Gene silencing mediated by dsRNA (RNAi) can persist for multiple generations in C. elegans (termed RNAi inheritance). Here we describe the results of a forward genetic screen in C. elegans that has identified six factors required for RNAi inheritance: GLH-1/VASA, PUP-1/CDE-1, MORC-1, SET-32, and two novel nematode-specific factors that we term here (heritable RNAi defective) HRDE-2 and HRDE-4. The new RNAi inheritance factors exhibit mortal germline (Mrt) phenotypes, which we show is likely caused by epigenetic deregulation in germ cells. We also show that HRDE-2 contributes to RNAi inheritance by facilitating the binding of small RNAs to the inheritance Argonaute (Ago) HRDE-1. Together, our results identify additional components of the RNAi inheritance machinery whose sequence conservation provides insights into the molecular mechanism of RNAi inheritance, further our understanding of how the RNAi inheritance machinery promotes germline immortality, and show that HRDE-2 couples the inheritance Ago HRDE-1 with the small RNAs it needs to direct RNAi inheritance and germline immortality.

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Project description:Transgenerational epigenetic inheritance and resetting of an environmentally-triggered change in gene expression in C. elegans

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Project description:Using Caenorhabditis elegans to investigate environmental cues-induced mitochondrial dysfunction, we found that exposure to electron transport chain (ETC) inhibitors at the parental generation initiates the transmission of heritable information to descendants and make descendants stress-adaptive. This mitochondrial stress adaptation phenotype can persist for at least three generations. Animals lacking histone H3K4me3 chromatin modifiers, or the methyltransferase of N6-methyldeoxyadenosine (6mA), lose the ability to initiate stress adaptation in progeny. H3K4me3 plays a role upstream of 6mA, while both mark promoter regions of mitochondrial unfolded protein response (UPR mt ) genes and activate the UPR mt pathway to alleviate mitochondrial damage.

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