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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of MCF-7 (breast adenocarcinoma) and 2102Ep (embryonic carcinoma) cells upon LINE-1 knockdown.

ABSTRACT: To measure the levels of expression of retrotransposon individual copies, and particularly of LINE-1 (L1) elements of the L1HS-Ta subfamily, we performed 2x150 bp paired-end and strand-specific RNA-seq on polyA+ RNA of MCF-7 and 2102Ep cells, which express high levels of L1. To confirm the origin of the L1-specific signal, we also performed RNA-seq upon shRNA-mediated L1 knockdown. sh960 relates to a scramble shRNA control. sh1083 and sh1085 relate to two distinct shRNAs directed against the ORF1 region of L1.3 (GenBank L19088) as a prototype L1HS-Ta.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Gael Cristofari

PROVIDER: E-MTAB-3788 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Activation of individual L1 retrotransposon instances is restricted to cell-type dependent permissive loci.

Philippe Claude C Vargas-Landin Dulce B DB Doucet Aurélien J AJ van Essen Dominic D Vera-Otarola Jorge J Kuciak Monika M Corbin Antoine A Nigumann Pilvi P Cristofari Gaël G

eLife 20160326

LINE-1 (L1) retrotransposons represent approximately one sixth of the human genome, but only the human-specific L1HS-Ta subfamily acts as an endogenous mutagen in modern humans, reshaping both somatic and germline genomes. Due to their high levels of sequence identity and the existence of many polymorphic insertions absent from the reference genome, the transcriptional activation of individual genomic L1HS-Ta copies remains poorly understood. Here we comprehensively mapped fixed and polymorphic ...[more]

PMID: 27016617

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A comprehensive map of L1HS-Ta retrotransposons in a panel of human cells obtained by ATLAS-seq.

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2016-05-24 | E-MTAB-4676 | biostudies-arrayexpress

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Project description:We used ATLAS-seq to comprehensively map the genomic location of LINE-1 elements belonging to the youngest and potentially polymorphic subfamily (L1HS-Ta). This was performed in single-cells of 2 preimplantation embryos (E3 and E6) as well as from the remaining inner cell mass (denoted T). In brief, single cells were isolated from the inner cell mass of preimplantation embryos by laser drilling and micromanipulation. Whole-genome Multiple Displacement Amplification was performed on each isolated single cells, as well as on the remaining cells of the inner cell mass as a population (samples labelled 'T'). Then we applied ATLAS-seq to map L1HS-Ta retrotransposons. This approach relies on the random mechanical fragmentation of the genomic DNA to ensure high-coverage, ligation of adapter sequences, suppression PCR-amplification of L1HS-Ta element junctions, and Ion Torrent sequencing using single-end 400 bp read chemistry. A notable aspect of ATLAS-seq is that we can obtain both L1 downstream and upstream junctions (3'- and 5'-ATLAS-seq libraries, respectively), for full-length L1 elements.

2023-09-30 | E-MTAB-8616 | biostudies-arrayexpress

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2021-12-15 | E-MTAB-10895 | biostudies-arrayexpress

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2023-09-23 | E-MTAB-12249 | biostudies-arrayexpress

RNA-seq of a panel of human normal and cancer cell lines

Project description:We performed poly(A)+ stranded RNA-seq of a panel of human primary or transformed cell lines (BJ, IMR90, MRC5, K562, HCT116, HeLa S3, HepG2, MCF7, HEK-293, HEK-293T, 2102Ep). In parallel, we determined the genomic location and DNA methylation levels of human full-length LINE-1 elements (L1) from the same cell lines using bs-ATLAS-seq (E-MTAB-10895). To link DNA methylation and L1 expression, we used cell pellets from the same cell culture to perform both RNA-seq and bs-ATLAS-seq.

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Genome-wide identification and DNA methylation of human full-length LINE-1 (L1) retrotransposons in a panel of embryonic stem cells, induced-pluripotent stem cells and their progenitor cells

Project description:We used bs-ATLAS-seq to comprehensively map the genomic location and assess the DNA methylation status of human full-length LINE-1 elements (L1). The approach is focused on the youngest family (L1HS), but it also catches a significant fraction of L1PA2 to L1PA8 elements. This was performed in a panel of embryonic stem cells, induced-pluripotent stem cells and their progenitor cells, at different passages.

2023-09-30 | E-MTAB-10904 | biostudies-arrayexpress

Genome-wide identification and DNA methylation of human full-length LINE-1 (L1) retrotransposons in HCT116 cells treated with 5-aza-2’-deoxycytidine.

Project description:We used bs-ATLAS-seq to comprehensively map the genomic location and assess the DNA methylation status of human full-length LINE-1 elements (L1). The approach is focused on the youngest family (L1HS), but it also catches a significant fraction of L1PA2 to L1PA8 elements. This was performed in HCT116 cells treated by the DNA methyltransferase inhibitor 5-aza-2’-deoxycytidine (5-aza) or in mock-treated cells (DMSO).

2023-09-22 | E-MTAB-12240 | biostudies-arrayexpress

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2023-05-10 | PXD039943 | Pride

Evollutionally dynamic L1 regulation in embryonic stem cells

Project description:Mobile elements are important evolutionary forces that challenge genomic integrity. Long interspersed element-1 (L1, also known as LINE-1) is the only autonomous transposon still active in the human genome. It displays an unusual pattern of evolution, with at any given time a single active L1 lineage amplifying to thousands of copies before getting replaced by a new lineage likely under pressure of host restriction factors, which act notably by silencing L1 expression during early embryogenesis. Here, we demonstrate that in human embryonic stem cells (hESC) KAP1, the master co-factor of KRAB-containing zinc finger proteins (KRAB-ZFP) previously implicated in the restriction of endogenous retroviruses, represses a discrete subset of L1 lineages predicted to have entered the ancestral genome between 26.8 and 7.6 million years ago. In the mouse, we documented a similar chronologically conditioned pattern, albeit with a much contracted time scale. We could further identify an L1-binding KRAB-ZFP, suggesting that this rapidly evolving protein family is more globally responsible for L1 recognition. KAP1 knockdown in hESC induced the expression of KAP1-bound L1 elements, but their younger, human-specific counterparts (L1Hs) were unaffected. Instead, they were stimulated by depleting DNA methyltransferases, consistent with recent evidence demonstrating that the PIWI-piRNA pathway regulates L1Hs in hESC. Altogether, these data indicate that the early embryonic control of L1 is an evolutionary dynamic process, and support a model whereby newly emerged lineages are first suppressed by DNA methylation-inducing small RNA-based mechanisms, before KAP1-recruiting protein repressors are selected. HA-tagged Gm6871 ChIP-seq in mES cells, RNA-seq in control and Gm6871 KD mES cells, KAP1 ChIP-seq in WT mES cells, RNA-seq in control and DNMTs KD hES cells.

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