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Caenorhabditis elegans

ABSTRACT: Untangling the Role of H3K9 Methylations in Transgenerational Small RNA Inheritance

PROVIDER: PRJNA374350 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5245490.fastq.gz	Fastqsanger.gz
	SRR5245500.fastq.gz	Fastqsanger.gz
	SRR5245510.fastq.gz	Fastqsanger.gz
	SRR5245520.fastq.gz	Fastqsanger.gz
	SRR5245530.fastq.gz	Fastqsanger.gz

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Project description:Some epigenetic modifications are inherited from one generation to the next, providing a potential mechanism for the inheritance of environmentally acquired traits. Transgenerational inheritance of RNA interference phenotypes in C. elegans provides an excellent model to study this phenomenon, and whilst studies have implicated both chromatin modifications and small RNA pathways in heritable silencing their relative contributions remain unclear. Here we demonstrate that the histone methyltransferases SET-25 and SET-32 are required for the establishment of a transgenerational silencing signal, but not for long-term maintenance of this signal between subsequent generations suggesting that transgenerational epigenetic inheritance is a multi-step process, with distinct genetic requirements for establishment and maintenance of heritable silencing. Furthermore, small RNA sequencing reveals that the abundance of secondary siRNA (thought to be the effector molecules of heritable silencing) does not correlate with silencing phenotypes. Together, our results suggest that the current mechanistic models of epigenetic inheritance are incomplete.

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Project description:Transgenerational changes in small RNA profiles of C.elegans mutants lacking PRG-1

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Untangling the Role of H3K9 Methylations in Transgenerational Small RNA Inheritance

Project description:In C.elegans, disruption of the chromatin landscape produces transgenerational effects, such as inherited increase in lifespan and gradual loss of fertility. Inheritance of histone modifications can be induced by double strand RNA-derived heritable small RNAs. We show that the mortal germline phenotype which is typical to met-2 mutants, defective in H3K9 methylation, depends on HRDE-1, an argonaute that carries small RNAs across generations, and is accompanied by accumulated transgenerational misexpression of heritable small RNAs. We discovered that MET-2 inhibits small RNA inheritance, and as a consequence, induction of RNAi in met-2 mutants leads to permanent RNAi responses that do not terminate even after more than 30 generations. We found that potentiation of heritable RNAi in met-2 animals results from global hyperactivation of the small RNA inheritance machinery. Thus, changes in histone modifications can give rise to drastic transgenerational epigenetic effects, by controlling the overall potency of small RNA inheritance.

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