Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1213312 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32058526_1.fastq.gz | Fastqsanger.gz | |||
| SRR32058526_2.fastq.gz | Fastqsanger.gz | |||
| SRR32058527_1.fastq.gz | Fastqsanger.gz | |||
| SRR32058527_2.fastq.gz | Fastqsanger.gz | |||
| SRR32058528_1.fastq.gz | Fastqsanger.gz |
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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:How artificial environmental cues are biologically integrated and transgenerationally inherited is still poorly understood. Here, we investigate the mechanisms of inheritance of reproductive outcomes elicited by the model environmental chemical Bisphenol A (BPA) in C. elegans. We show that BPA exposure causes the derepression of an epigenetically silenced transgene in the germline for 5 generations, regardless of ancestral response. ChIP-seq, histone modifications quantitation, and immunofluorescence assays revealed that this effect is associated with a reduction of the repressive marks H3K9me3 and H3K27me3 in whole worms and in germline nuclei in the F3 as well as with reproductive dysfunctions including germline apoptosis and embryonic lethality. Furthermore, targeting of the Jumonji demethylases JMJD-2 and JMJD-3/UTX-1 restores H3K9me3 and H3K27me3 levels, respectively, and fully alleviates the BPA-induced transgenerational effects. Together, our results demonstrate the central role of repressive histone modifications in the inheritance of reproductive defects elicited by a common environmental chemical exposure.
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