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LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay
LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay
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LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay
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LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay
LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay

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LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay
LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay
Journal Article

LSM2-8 and XRN-2 contribute to the silencing of H3K27me3-marked genes through targeted RNA decay

2020
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Overview
In fission yeast and plants, RNA processing and degradation contribute to heterochromatin silencing, alongside conserved pathways of transcriptional repression. It has not been known whether similar pathways exist in metazoans. Here, we describe a pathway of silencing in Caenorhabditis elegans somatic cells, in which the highly conserved RNA-binding complex LSM2-8 contributes selectively to the repression of heterochromatic reporters and endogenous genes bearing the Polycomb mark, histone H3K27me3. This acts by degrading selected transcripts through the XRN-2 exoribonuclease. Disruption of the LSM2-8 pathway leads to mRNA stabilization. Unlike previously described pathways of heterochromatic RNA degradation, LSM2-8-mediated RNA degradation does not target nor require H3K9 methylation. Intriguingly, loss of this pathway coincides with a localized reduction in H3K27me3 at lsm-8-sensitive loci. We have thus uncovered a mechanism of RNA degradation that selectively contributes to the silencing of a subset of H3K27me3-marked genes, revealing a previously unrecognized layer of post-transcriptional control in metazoan heterochromatin.Mattout et al. show that the nuclear LSM2-8 complex acts with the exonuclease XRN-2 to degrade transcripts of H3K27me3-marked genes, thus facilitating gene silencing.