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Atypical mitotic DNA synthesis sequencing (MiDAS-seq) in U2OS cells depleted for RAD51

ABSTRACT: Atypical mitotic DNA synthesis sequencing (MiDAS-seq) in U2OS cells depleted for RAD51

PROVIDER: PRJNA804143 | ENA |

REPOSITORIES: ENA

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Atypical mitotic DNA synthesis sequencing (MiDAS-seq) in U2OS cells depleted for RAD51

Project description:DNA replication stress is an established driver of cancer-associated chromosomal rearrangements. Replication stress perturbs the duplication of late-replicating loci and activates a mitotic DNA repair pathway (termed MiDAS) for completion of replication. We here investigated RAD51-independent MiDAS.

2022-06-27 | GSE196278 | GEO

The nascent transcriptome during G1, Early-s, Late-S, and G2/M cell cycle phases and atypical MiDAS-seq in RAD51 knockdown U2OS cells

Project description:The nascent transcriptome during G1, Early-s, Late-S, and G2/M cell cycle phases and atypical MiDAS-seq in RAD51 knockdown U2OS cells

| PRJNA804140 | ENA

MiDAS in BRCA2-deficient cells originate at early S-phase transcription-replication conflicts

Project description:Multiple replication abnormalities cause cells lacking BRCA2 to enter mitosis with under-replicated DNA and to activate mitotic DNA synthesis (MiDAS). However, the precise position of these MiDAS sites, as well as their origin, remains unknown. Here we labelled mitotic nascent DNA and performed high-throughput sequencing to identify at high-resolution the sites where MiDAS occurs in the absence of BRCA2. This approach revealed 150 genomic loci affected by MiDAS, which map within regions replicating during early S-phase and are therefore distinct from the aphidicolin-induced common fragile sites. Moreover, these sites largely localise near early firing origins and within genes transcribed in early S, suggesting that they stem from transcription-replication conflicts (TCRs). Inhibiting transcription with 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole (DRB) during early S-phase abrogates MiDAS. Strikingly, MiDAS sites co-localise with genomic loci where R-loops form in unchallenged conditions, suggesting that R-loop accumulation caused by BRCA2 inactivation leads to DNA lesion which are repaired by MiDAS. RAD52 is required in this process, as its abrogation in BRCA2-deficient cells reduces the rate of MiDAS and causes DNA damage accumulation in G1. Furthermore, MiDAS sites triggered by BRCA2 inactivation are hotspots for genomic rearrangement in BRCA2-mutated breast tumours. These results indicate that BRCA2 acts in early S-phase to protect TRC- and R-loop-induced DNA lesions, thereby preventing them from becoming a source of genomic instability and tumorigenesis.

2022-08-01 | GSE196163 | GEO

Midas v5

Project description:Midas genome assembly version 5

| PRJEB6974 | ENA

The nascent transcriptome during G1, Early-s, Late-S, and G2/M cell cycle phases and atypical MiDAS-seq in RAD51 knockdown U2OS cells

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

2022-06-27 | GSE196279 | GEO

MiDAS-DK

Project description:The microbial database of activated sludge - Denmark (MiDAS-DK)

| PRJEB8105 | ENA

U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2

Project description:U2OS-ERa, U2OS-ERb, and U2OS-ERab cells treated with 4HT or E2 Keywords: other

2005-04-06 | GSE2292 | GEO

The inability to disassemble Rad51 nucleoprotein filaments leads to aberrant mitosis and cell death

Project description:The proper maintenance of genetic material is essential for the survival of living organisms. One of the main safeguards of genome stability is homologous recombination involved in the faithful repair of DNA double-strand breaks, the restoration of collapsed replication forks, and the bypass of replication barriers. Homologous recombination relies on the formation of Rad51 nucleofilaments which are responsible for the homology-based interactions between DNA strands. Here we demonstrate that without the regulation of these filaments by Srs2 and Rad54, which are known to remove Rad51 from single-stranded and double-stranded DNA respectively, the filaments strongly inhibit damage-associated DNA synthesis during DNA repair. Furthermore, this regulation is essential for cell survival under normal growth conditions as in the srs2Δ rad54Δ mutants unregulated Rad51 nucleofilaments cause activation of the DNA damage checkpoint, formation of mitotic bridges and loss of genetic material. These genome instability features may stem from the problems at stalled replication forks as the lack of Srs2 and Rad54 in the presence of Rad51 nucleofilaments impedes cell recovery from replication stress. This study demonstrates that the timely and efficient disassembly of recombination machinery is essential for genome maintenance and cell survival.

2023-03-16 | GSE227383 | GEO

Expression data from SKOV3.ip cells by knockdown RAD51-AS1 expression.

Project description:Long non-coding RNAs (lncRNA) have been shown to play crucial roles in tumorigenesis. Little is known about lncRNA RAD51-AS1 in diseases. Here, we investigated the role of RAD51-AS1 in Epithelial ovarian cancer. Silencing RAD51-AS1 inhibited proliferation through cell cycle arrest and promotion in apoptosis, both in vitro and in vivo. But the mechanism of RAD51-AS1 downstream regulation remains unclear. In order to identify the downstream regulation of RAD51-AS1 in epithelial ovarian cancer, we used antisene oligotides targeting RAD51-AS1 / negative control to transfect Skov3.ip cells. Then, we used microarrays to identified differential expression genes and to look for possible target genes by knockdown RAD51-AS1 expression.

2017-08-17 | GSE89374 | GEO

RAD51 Interconnects Between DNA Replication, DNA Repair and Immunity

Project description:RAD51, a multifunctional protein, plays a central role in DNA replication and homologous recombination repair, and is known to be involved in cancer development. We identified a novel role for RAD51 in innate immune response signaling. Defects in RAD51 lead to the accumulation of self-DNA in the cytoplasm, triggering a STING-mediated innate immune response after replication stress and DNA damage. Our data suggest that in addition to playing roles in homologous recombination-mediated DNA double-strand break repair and replication fork processing, RAD51 is also implicated in the suppression of innate immunity. Thus, our study reveals a previously uncharacterized role of RAD51 in initiating immune signaling, placing it at the hub of new interconnections between DNA replication, DNA repair, and immunity.

2017-02-18 | GSE95050 | GEO

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