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

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

PROVIDER: PRJNA804140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17914843.fastq.gz	Fastqsanger.gz
	SRR17914844.fastq.gz	Fastqsanger.gz
	SRR17914845.fastq.gz	Fastqsanger.gz
	SRR17914846.fastq.gz	Fastqsanger.gz
	SRR17914847.fastq.gz	Fastqsanger.gz

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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

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

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

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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

Expression profiling of HeLa cells at S and G2/M phases of mitotic cell cycle.

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Expression profiling of HeLa cells at S and G2/M phases of mitotic cell cycle.

Project description:We compared the mRNAs expression profile of HeLa cells between two phases of the mitotic cell cycle: S and G2/M phases. Results provide insight into the regulation of transcript levels during mitotic cell cycle progression. HeLa cells were synchronized with double thymidine blockade (12 hours with 2 mM thymidine, 12 hours release, and 12 hours with 2 mM thymidine), and cells were taken after 2 hours release (S phase) and 8 hours release (G2/M phase). Keywords: time course Comparison of mRNAs measured at S phase (2 hours release after double thymidine blockade) and at G2/M phase (8 hours release after double thymidine blockade); 3 biological replicates at each of the two time points; two technical replicates with dye swapping per comparison; additional comparison between G2/M (8h) and S (2h).

2010-05-07 | E-GEOD-15547 | biostudies-arrayexpress

BCR-ABL is enriched in S- and G2-cell cycle phases

Project description:To address the unusually long duration of imatinib therapy for chronic myelogenous leukemia, we sought to understand the expression of BCR-ABL gene expression with different phases of the cell cycle. A precedent for dynamic fusion oncoprotein expression already exists for the pediatric solid tumor, rhabdomyosarcoma. Quantitative immunocytochemistry was conducted to compare the expression of BCR-ABL with markers of each cell cycle phase: CDK6 for G1, CDK2 for S, phospho-CDC2 for G2, and phospho-HH3 for M phase. BCR-ABL expression was most strongly correlated with the G2 and S cell cycle phases. Low BCR-ABL expression only coincided with high cell cycle marker expression for the G1. BCR-ABL was rarely if at all expressed in M. Our results suggest a possible explanation for the prolonged nature of imatinib therapy, which may be only effective on S- and G2-phase actively replicating leukemia cells.

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RPA accumulation during class switch recombination represents 5'-3' DNA end resection during the S-G2/M phase of the cell cycle

Project description:AID promotes chromosomal translocations by inducing DNA double-strand breaks (DSBs) at immunoglobulin (Ig) genes and oncogenes in G1. RPA is a ssDNA-binding protein that associates with resected DSBs in the S phase and facilitates the assembly of factors involved in homologous repair (HR) such as Rad51. Notably, RPA deposition also marks sites of AID-mediated damage, but its role in Ig gene recombination remains unclear. Here we demonstrate that RPA associates asymmetrically with resected ssDNA in response to lesions created by AID, RAG, or other nucleases. Small amounts of RPA are deposited at AID targets in G1 in an ATM-dependent manner. In contrast, recruitment in S-G2/M is extensive, ATM-independent, and associated with Rad51 accumulation. RPA in S-G2/M increases in NHEJ-deficient lymphocytes, where there is more extensive DNA-end resection. Thus, most RPA recruitment during CSR represents salvage of un-repaired breaks by homology-based pathways during the S-G2/M phases of the cell cycle. Chip-Seq of RPA from mouse activated B cells (n = 40), mouse thymocytes (n = 6), and MEFs (n = 1). Different genotypes and/or inhibitors were used.

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RPA accumulation during class switch recombination represents 5'-3' DNA end resection during the S-G2/M phase of the cell cycle

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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