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Germline- and soma-specific heritable epigenetic silencing at an endogenous locus

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE81708 | GEO | 2017/02/16

SECONDARY ACCESSION(S): PRJNA322336

REPOSITORIES: GEO

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Germline- and soma-specific heritable epigenetic silencing at an endogenous locus (RNA-Seq)

Project description:The emergence and transmission of epigenetic signals across generations can quickly and efficiently alter gene expression in a population. We describe an epigenetic silencing signal whose initiation, transmission properties, genetic requirements and site of action are distinct from previously described epigenetic inheritance in C. elegans. A multi-copy transgene containing the region upstream of sid-1 silences sid-1 and upstream genes. Once established, silencing is stable in the absence of the array and can be maintained without selection for 13 generations. We show that the silenced state can be transmitted to progeny in the absence of the silenced locus, but that inherited silencing is dependent on the nuclear RNAi Argonaute HRDE-1, which stabilizes silencing siRNAs that target sid-1 exons. Notably, at each generation, the RNAi-dependent germline silenced sid-1 locus transitions to a chromatin-dependent silenced state in somatic cells, indicating that the mechanisms of transgenerational silencing in the soma and germline are distinct.

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Germline- and soma-specific heritable epigenetic silencing at an endogenous locus (small RNA-Seq)

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Germline- and soma-specific heritable epigenetic silencing at an endogenous locus

Project description:Germline- and soma-specific heritable epigenetic silencing at an endogenous locus

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Stable Heritable Germline Silencing Directs Somatic Silencing at an Endogenous Locus.

Project description:The importance of transgenerationally inherited epigenetic states to organismal fitness remains unknown as well-documented examples are often not amenable to mechanistic analysis or rely on artificial reporter loci. Here we describe an induced silenced state at an endogenous locus that persists, at 100% transmission without selection, for up to 13 generations. This unusually persistent silencing enables a detailed molecular genetic analysis of an inherited epigenetic state. We find that silencing is dependent on germline nuclear RNAi factors and post-transcriptional mechanisms. Consistent with these later observations, inheritance does not require the silenced locus, and we provide genetic evidence that small RNAs embody the inherited silencing signal. Notably, heritable germline silencing directs somatic epigenetic silencing. Somatic silencing does not require somatic nuclear RNAi but instead requires both maternal germline nuclear RNAi and chromatin-modifying activity. Coupling inherited germline silencing to somatic silencing may enable selection for physiologically important traits.

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C. elegans establishes germline versus soma by balancing inherited histone methylation

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:To define what genes are predominantly or specifically expressed in either soma or germline in C. elegans adults, total RNA was extracted from germline-less glp-4 mutant animals or from dissected gonads, respectively. Total RNA sequencing was peformed in duplicates. Four samples in total.

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Epigenetic transitions leading to heritable, RNA-mediated de novo silencing in Arabidopsis thaliana.

Project description:In plants, RNA-directed DNA methylation (RdDM), a mechanism where epigenetic modifiers are guided to target loci by small RNAs, plays a major role in silencing of transposable elements (TEs) to maintain genome integrity. So far, two RdDM pathways have been identified: RNA Polymerase IV (PolIV)-RdDM and RNA-dependent RNA Polymerase 6 (RDR6)-RdDM. PolIV-RdDM involves a self-reinforcing feedback mechanism that maintains TE silencing, but cannot explain how epigenetic silencing is first initiated. A function of RDR6-RdDM is to reestablish epigenetic silencing of active TEs, but it is unknown if this pathway can induce DNA methylation at naïve, non-TE loci. To investigate de novo establishment of RdDM, we have used virus-induced gene silencing (VIGS) of an active flowering Wageningen epiallele. Using genetic mutants we show that unlike PolIV-RdDM, but like RDR6-RdDM, establishment of VIGS-mediated RdDM requires PolV and DRM2 but not Dicer like-3 and other PolIV pathway components. DNA methylation in VIGS is likely initiated by a process guided by virus-derived small (s) RNAs that are 21/22-nt in length and reinforced or maintained by 24-nt sRNAs. We demonstrate that VIGS-RdDM as a tool for gene silencing can be enhanced by use of mutant plants with increased production of 24-nt sRNAs to reinforce the level of RdDM.

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