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Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [CHART-Seq]

ABSTRACT: In the developing mouse embryo, expression of the lncRNA Airn induces gene silencing and recruits Polycomb Repressive Complexes (PRCs) to varying extents over a 15 megabase domain, but the mechanisms remain unclear. Using high-resolution approaches, we show in mouse trophoblast stem cells that Airn expression induces long-range changes to chromatin architecture centered around a network of CpG islands occupied by PRCs and SMC1A/Cohesin. Extent of contact with Airn predicts underlying intensity of Polycomb-directed chromatin modifications and Airn-induced changes to chromatin architecture. Deletion of individual CpG islands alternately increase or decrease gene silencing and PRC activity over the domain in a manner predicted by changes in chromatin architecture. We conclude that Airn is a potent repressive lncRNA whose effects are controlled by an equilibratory network of DNA regulatory elements that modulate its frequency of contact with target chromatin.

ORGANISM(S): Mus musculus

PROVIDER: GSE217261 | GEO | 2023/07/01

REPOSITORIES: GEO

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Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [Hi-C]

Project description:In the developing mouse embryo, expression of the lncRNA Airn induces gene silencing and recruits Polycomb Repressive Complexes (PRCs) to varying extents over a 15 megabase domain, but the mechanisms remain unclear. Using high-resolution approaches, we show in mouse trophoblast stem cells that Airn expression induces long-range changes to chromatin architecture centered around a network of CpG islands occupied by PRCs and SMC1A/Cohesin. Extent of contact with Airn predicts underlying intensity of Polycomb-directed chromatin modifications and Airn-induced changes to chromatin architecture. Deletion of individual CpG islands alternately increase or decrease gene silencing and PRC activity over the domain in a manner predicted by changes in chromatin architecture. We conclude that Airn is a potent repressive lncRNA whose effects are controlled by an equilibratory network of DNA regulatory elements that modulate its frequency of contact with target chromatin.

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Project description:Long noncoding RNAs (lncRNAs) cause Polycomb Repressive Complexes (PRCs) to spread over broad regions of the mammalian genome. We report that in mouse trophoblast stem cells, the Kcnq1ot1 and Airn lncRNAs induce PRC-dependent chromatin modifications over multi-megabase domains. Throughout the Airn-targeted domain, extent of PRC-dependent modification correlated with intra-nuclear distance to the Airn locus, pre-existing genome architecture, and the abundance of Airn itself. Specific CpG islands displayed characteristics indicating that they nucleate the spread of PRCs upon exposure to Airn. Chromatin environments surrounding Xist, Airn, and Kcnq1ot1 suggest common mechanisms of PRC engagement and spreading. Our data indicate that lncRNA potency can be tightly linked to lncRNA abundance, and that within lncRNA-targeted domains, PRCs are recruited to CpG islands via lncRNA-independent mechanisms. We propose that CpG islands that autonomously recruit PRCs interact with lncRNAs and their associated proteins through 3-dimensional space to nucleate the spread of PRCs in lncRNA-targeted domains.

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Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [CHART-Seq]

Project description:Proximity-dependent recruitment of Polycomb Repressive Complexes by the lncRNA Airn [CHART-Seq]

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Airn transcriptional overlap but not its lncRNA products induce imprinted Igf2r silencing.

Project description:To test if the imprinted long non-coding RNA (lncRNA) Airn transcription or its product silences the protein-coding Igf2r gene, we shortened the endogenous lncRNA to four different lengths by inserting polyadenylation (polyA) cassettes on the paternal chromosome via homologous recombination in ES cells. ES cell differentiation was used to recapitulate the developmental onset of Airn and Igf2r imprinted expression and polyA cassettes inserted before (T3, T16, T27) or after (T31, T51) the Igf2r promoter successfully truncated Airn, with the exception of T27. RNA hybridization to a tiling array (MIRTA) demonstrated loss of Airn upstream of the Igf2r promoter (except T27) and absence of novel spliced variants in all truncation alleles. To further test the transcriptional overlap model we moved the Airn promoter ~700bp before the Igf2r TSS in ES cells that lack an endogenous paternal Airn promoter and called this cell line FAP (Forward-Airn-Promoter). RNA hybridization to a tiling array (MIRTA) demonstrated that the moved Airn promoter expresses Airn in wildtype orientation and terminates at the wildtype 3' end. ES cell lines expressing different Airn variants were differentiated on gelatinized dishes after feeder cell depletion and LIF withdrawal by 0.27M-BM-5M retinoic acid for 5 days and Airn length was assayed.

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KDM2B binds CpG islands and modulates recruitment of Ring1b

Project description:CpG island elements are associated with most mammalian gene promoters, yet how they contribute to gene regulation remains poorly understood. Recently it has become clear that a subset of CpG islands in embryonic stem cells can act as polycomb response elements and are recognized by the polycomb silencing systems to regulate the expression of genes involved in pluripotency and early developmental transcription programs. How CpG islands function mechanistically as nucleation sites for polycomb repressive complexes remains unknown. Here we discover that the KDM2B protein, by virtue of its ZF-CxxC DNA binding domain, specifically recognizes non-methylated DNA in CpG islands elements genome-wide. Through a physical interaction with the polycomb repressive complex 1 (PRC1), KDM2B targets PRC1 to CpG islands where it contributes to H2AK119ub1 and gene repression at a subset of polycomb targets. Unexpectedly, we also find that CpG islands are occupied by low levels of PRC1 throughout the genome, suggesting that the KDM2B-PRC1 complex may sample CpG island associated genes for susceptibility to polycomb mediated silencing. These observations demonstrate an unexpected and direct link between recognition of CpG islands by KDM2B and targeting of the polycomb repressive system. This provides the basis for a new model describing the functionality of CpG islands as mammalian PREs.

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