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ABSTRACT: An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility

PROVIDER: PRJNA1202082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31826012_1.fastq.gz	Fastqsanger.gz
	SRR31826013_1.fastq.gz	Fastqsanger.gz
	SRR31826014_1.fastq.gz	Fastqsanger.gz
	SRR31826015_1.fastq.gz	Fastqsanger.gz
	SRR31826016_1.fastq.gz	Fastqsanger.gz

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An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility

Project description:An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility

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An endogenous retroviral element co-opts an upstream regulatory sequence to achieve somatic expression and mobility

Project description:We characterize somatic retrotransposition in the Drosophila intestine using long-read DNA sequencing. We show that retroelement mobility does not change significantly upon aging and is limited to very few active sub-families of retrotransposons. Importantly, we identify a polymorphic donor locus of an endogenous LTR retroviral element rover, active in the intestinal tissue. We reveal that gut activity of the rover donor copy depends on its genomic environment. Without affecting local gene expression, the copy co-opts its upstream enhancer sequence, rich in transcription factor binding sites, for somatic expression. We further show that escargot, a snail-type transcription factor critical for gut progenitor cell function, can drive transcriptional activity of the active rover copy. These data provide new insights into how locus-specific features allow active retrotransposons to produce functional transcripts and mobilize in a somatic lineage.

2024-12-26 | GSE285324 | GEO

Project description:Histone H3.3 is required for endogenous retroviral element silencing and genome stability

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Project description:Suppression of endogenous retroviral enhancers in somatic cell nuclear transfer embryos

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The Vasa homolog RDE-12 engages target mRNA and a secondary-Argonaute WAGO-1 to promote RNAi in C. elegans

Project description:Argonaute proteins (AGOs) are key nuclease effectors of RNA interference (RNAi) [1]. Although purified AGOs can mediate a single round of target-RNA cleavage in vitro, accessory factors are required for siRNA loading and to achieve multiple-target turnover [2, 3]. To identify AGO co-factors we immunoprecipitated the C. elegans AGO WAGO-1, which engages amplified small RNAs during RNAi [4]. These studies identified a robust association between WAGO-1 and a conserved Vasa ATPase-related protein RDE-12. rde-12 mutants are deficient in RNAi including viral suppression, and fail to produce amplified secondary siRNAs and certain endogenous siRNAs (endo-siRNAs). RDE-12 co-localizes with WAGO-1 in germline P-granules and to peri-nuclear cytoplasmic foci in somatic cells. These findings and our genetic studies suggest that (i) RDE-12 is first recruited to target mRNAs by upstream AGOs (RDE-1 and ERGO-1) where it promotes small-RNA amplification and/or WAGO-1 loading, and that (ii) downstream of these events, RDE-12 forms an RNase-resistant (target mRNA-independent) complex with WAGO-1 that may scan for additional target mRNAs. Examine small RNA population changes in rde-12 mutants

2014-06-24 | E-GEOD-54396 | biostudies-arrayexpress

An Oncogenic Super-Enhancer Formed through Somatic Mutation of a Noncoding Intergenic Element

Project description:In many cancers, critical oncogenes are driven from large regulatory elements, called super-enhancers, which recruit much of the cellM-bM-^@M-^Ys transcriptional apparatus and are defined by extensive H3K27 acetylation. We found that in T-cell acute lymphoblastic leukemia (T-ALL), somatic heterozygous mutations introduce MYB binding motifs in a precise noncoding site, which nucleate a super-enhancer upstream of the TAL1 oncogene. Further analysis of genome-wide binding identified MYB and its histone acetylase binding partner CBP as core components of the TAL1 complex and of the TAL1-mediated feed-forward auto-regulatory loop that drives T-ALL. Furthermore, MYB and CBP occupy endogenous MYB binding sites in the majority of super-enhancer sites found in T-ALL cells. Thus, our study reveals a new mechanism for the generation of super-enhancers in malignant cells involving the introduction of somatic indel mutations within non-coding sequences, which introduce aberrant binding sites for the MYB master transcription factor. ChIP-Seq for transcription factors and co-factors in T cell acute lymphoblastic leukemia cell lines

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Mus musculus

Project description:Histone H3.3 is required for endogenous retroviral element silencing and genome stability [ChIP-Seq]

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DNMT and HDAC inhibition induces immunogenic neoantigens from human endogenous retroviral element-derived transcripts

Project description:DNMT and HDAC inhibition induces immunogenic neoantigens from human endogenous retroviral element-derived transcripts

| PRJNA862442 | ENA

Mus musculus

Project description:Histone H3.3 is required for endogenous retroviral element silencing and genome stability [RNA-Seq]

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Enhancer adoption by an LTR retrotransposon generates viral-like particles causing developmental limb phenotypes

Project description:Mammalian genomes are scattered with transposable elements (TEs). Silencing of TEs prevents harmful effects caused by either global activation leading to genome instability or insertional mutation disturbing gene transcription. However, whether the activation of a TE can be pathological without directly affecting gene expression is largely unknown. Here, we show that a TE insertion can adopt nearby regulatory activity, producing cell-type-specific viral-like particles (VLPs) in the embryo and affecting organ formation. Failure to silence an LTR retrotransposon inserted upstream of the Fgf8 gene results in their co-expression during development. VLPs assembly in the Fgf8-expressing cells of the developing limb triggers apoptotic cell death, resulting in a limb malformation resembling human ectrodactyly. We rescued this phenotype with mutations in the retrotransposon coding sequence, preventing its full endogenous retroviral cycle. Our findings illustrate how TE insertion is incorporated into the local genomic regulatory landscape and show that VLP production in post-implantation embryos can be pathological.

2025-03-15 | GSE246755 | GEO

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