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Mouse SINE B2 elements function as IFN-inducible enhancer elements [CUT&Tag]

ABSTRACT: B2_Mm2 acts as a STAT1 binding site and interferon inducible enhancer of the nearbby interferon-stimulated gene Dicer1 during an innate immune response (IFNG stimulated). J774 knockouts deficient of B2_Mm2 were also found to have downregulated expression of Serpina3f and Serpina3g, indicating that B2_Mm2 acts as an enhancer on these nearby genes likely due to its capability as a CTCF-binding site.

ORGANISM(S): Mus musculus

PROVIDER: GSE202572 | GEO | 2022/05/30

REPOSITORIES: GEO

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Mouse SINE B2 elements function as IFN-inducible enhancer elements [RNA-Seq]

Project description:B2_Mm2 acts as a STAT1 binding site and interferon inducible enhancer of the nearbby interferon-stimulated gene Dicer1 during an innate immune response (IFNG stimulated). J774 knockouts deficient of B2_Mm2 were also found to have downregulated expression of Serpina3f and Serpina3g, indicating that B2_Mm2 acts as an enhancer on these nearby genes likely due to its capability as a CTCF-binding site.

2022-05-30 | GSE202573 | GEO

Mouse B2 SINE elements function as IFN-inducible enhancers.

Project description:Regulatory networks underlying innate immunity continually face selective pressures to adapt to new and evolving pathogens. Transposable elements (TEs) can affect immune gene expression as a source of inducible regulatory elements, but the significance of these elements in facilitating evolutionary diversification of innate immunity remains largely unexplored. Here, we investigated the mouse epigenomic response to type II interferon (IFN) signaling and discovered that elements from a subfamily of B2 SINE (B2_Mm2) contain STAT1 binding sites and function as IFN-inducible enhancers. CRISPR deletion experiments in mouse cells demonstrated that a B2_Mm2 element has been co-opted as an enhancer driving IFN-inducible expression of Dicer1. The rodent-specific B2 SINE family is highly abundant in the mouse genome and elements have been previously characterized to exhibit promoter, insulator, and non-coding RNA activity. Our work establishes a new role for B2 elements as inducible enhancer elements that influence mouse immunity, and exemplifies how lineage-specific TEs can facilitate evolutionary turnover and divergence of innate immune regulatory networks.

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Mouse SINE B2 elements function as IFN-inducible enhancer elements

Project description:Mouse SINE B2 elements function as IFN-inducible enhancer elements

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Mouse SINE B2 elements function as IFN-inducible enhancer elements

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

2022-05-30 | GSE202574 | GEO

Mouse SINE B2 elements function as IFN-inducible enhancer elements [CUT&Tag]

Project description:Mouse SINE B2 elements function as IFN-inducible enhancer elements [CUT&Tag]

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Mouse SINE B2 elements function as IFN-inducible enhancer elements [RNA-Seq]

Project description:Mouse SINE B2 elements function as IFN-inducible enhancer elements [RNA-Seq]

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Murine Warriors or Worriers: The Saga of Comt1, B2 SINE Elements, and the Future of Translational Genetics.

Project description: Not available

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Next generation sequencing of MA-10 mouse Leydig tumor cells facilitates quantitative analysis of SINE B2-antisense transcripts with the RNAi system: wild type and Dicer1-knockdown transcriptomes

Project description:We report the comparison between SINE B2-AS transcriptome profiling and Dicer1-deficient-cell transcriptome profiling using RNA-seq analysis. We report that thousands of SINE B2 copies encode long B2-AS transcripts, which are constantly degraded by Dicer1. This new class of B2-AS transcripts regulates the expression of SINE B2 sense (B2-S) transcripts. Long B2-S is the main cause of cellular toxicity likely mediated by the multifunctional protein TSPO. Some B2-AS transcripts are putative miRNAs interconnected with the RNAi system. We propose that B2-AS transcripts have evolved as a self-defense mechanism to subvert the host RNAi system.

2020-09-01 | GSE126041 | GEO

B2 SINE expression during MHV68 infecton

Project description:Short interspersed nuclear elements (SINEs) are retrotransposons evolutionarily derived from endogenous RNA Polymerase III RNAs. Though SINE elements have undergone exaptation into gene regulatory elements, how transcribed SINE RNA impacts transcriptional and post-transcriptional regulation is largely unknown. This is partly due to a lack of information regarding which of the loci have transcriptional potential. Here, we present an approach (short interspersed nuclear element sequencing, SINE-seq), which selectively profiles RNA Polymerase III-derived SINE RNA, thereby identifying transcriptionally active SINE loci. Applying SINE-seq to monitor murine B2 SINE expression during a gammaherpesvirus infection revealed transcription from 28,270 SINE loci, with ~50% of active SINE elements residing within annotated RNA Polymerase II loci. Furthermore, B2 RNA can form intermolecular RNA-RNA interactions with complementary mRNAs, leading to nuclear retention of the targeted mRNA via a mechanism involving p54nrb. These findings illuminate a pathway for the selective regulation of mRNA export during stress via retrotransposon activation.

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Gene Conversion amongst Alu SINE Elements.

Project description:The process of non-allelic gene conversion acts on homologous sequences during recombination, replacing parts of one with the other to make them uniform. Such concerted evolution is best described as paralogous ribosomal RNA gene unification that serves to preserve the essential house-keeping functions of the converted genes. Transposed elements (TE), especially Alu short interspersed elements (SINE) that have more than a million copies in primate genomes, are a significant source of homologous units and a verified target of gene conversion. The consequences of such a recombination-based process are diverse, including multiplications of functional TE internal binding domains and, for evolutionists, confusing divergent annotations of orthologous transposable elements in related species. We systematically extracted and compared 68,097 Alu insertions in various primates looking for potential events of TE gene conversion and discovered 98 clear cases of Alu-Alu gene conversion, including 64 cases for which the direction of conversion was identified (e.g., AluS conversion to AluY). Gene conversion also does not necessarily affect the entire homologous sequence, and we detected 69 cases of partial gene conversion that resulted in virtual hybrids of two elements. Phylogenetic screening of gene-converted Alus revealed three clear hotspots of the process in the ancestors of Catarrhini, Hominoidea, and gibbons. In general, our systematic screening of orthologous primate loci for gene-converted TEs provides a new strategy and view of a post-integrative process that changes the identities of such elements.

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