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Genome-wide maps of FANCD2 binding sites in untreated and aphidicolin-treated HCT116 cells.

ABSTRACT: Analysis of FANCD2 targeted sequences and identification DNA motifs regulating transcription of large genes at common fragile sites.

ORGANISM(S): Homo sapiens

PROVIDER: GSE141101 | GEO | 2021/02/03

REPOSITORIES: GEO

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Genome-wide maps of FANCD2 binding sites in untreated and aphidicolin-treated HCT116 cells.

Project description:Genome-wide maps of FANCD2 binding sites in untreated and aphidicolin-treated HCT116 cells.

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Chromatin immunopreciptiation of human lymphoblastoid untreated and treated with aphidicolin (APH), trichostatin A (TSA), or APH plus TSA cells to map the origins of DNA replication at common fragile sites

Project description:Map the origins of DNA replication in human cells at 7 common fragile sites and their flanking non-fragile sequences as well as a 200kb containing the rare fragile site FRAXA, and a 1,075kb non-fragile region on chr22 . The origins were mapped in untreated cells, as well as, in cells treated with aphidicolin (APH), trichostatin A (TSA), or APH plus TSA. The origin mapping experiment is based on the fact that during S phase, short newly replicated DNA fragments (300bp-1kb) are generated only at the origins of replication. By combining the nascent strand assay with a tiled microarray platform, we have previoulsy developed a rapid, non-PCR based, high-throughput approach to map active origins in asynchronous human cells (Lucas et al., 2007, AC 17668008).

2010-02-27 | E-TABM-348 | biostudies-arrayexpress

FANCD2 Activates Transcription of TAp63 and Suppresses Tumorigenesis

Project description:Fanconi Anemia (FA) is a rare genetic disorder characterized by an increased susceptibility to squamous cell cancers. Fifteen FA genes are known, and the encoded proteins cooperate in a common DNA repair pathway. A critical step is the monoubiquitination of the FANCD2 protein, and cells from most FA patients are deficient in this step. How monoubiquitinated FANCD2 suppresses squamous cell cancers is unknown. Here we show that Fancd2-deficient mice are prone to Ras oncogene-driven skin carcinogenesis, while Usp1-deficient mice, expressing elevated cellular levels of Fancd2-Ub, are resistant to skin tumors. Moreover, Fancd2-Ub activates the transcription of the tumor suppressor TAp63, thereby promoting cellular senescence and blocking skin tumorigenesis. For FA patients, the reduction of FANCD2-Ub and TAp63 protein levels may account for their susceptibility to squamous cell neoplasia. Taken together, Usp1 inhibition may be a useful strategy for upregulating TAp63 and preventing or treating squamous cell cancers in the general non-FA population. Examination of FANCD2 binding after UV treatment in 293T cells

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Next Generation Sequencing Facilitates Quantitative Analysis of ChIP-sequence of U2OS cells expressing FANCD2-3x FLAG under mild replication stress by low dose aphidicolin (APH)

Project description:Genome-wide distribution of FANCD2 protein in chromatin under replication stress.

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FANCD2 Activates Transcription of TAp63 and Suppresses Tumorigenesis

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Effect of SRSF1 depletion on FANCD2 mRNA and isoform expression and effect of FANCD2 depletion or expression of SRSF1 mutants on splicing

Project description:To investigate the cooperative function of FANCD2/SRSF1 complex in the regulation of R-loops, we performed gene expression, isoform and splicing analysis in Hela cells depleted of SRSF1 or expressing SRSF1 mutants and FA-D2 mutant (FA-D2) and wild type (FA-D2+FANCD2) cells.

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FBXL12 degrades FANCD2 to regulate replication recovery and promote cancer cell survival under conditions of replication stress

Project description:Oncogene-induced replication stress constitutes an early obstacle for pre-cancerous cells to overcome to progress towards malignancy. Fanconi anaemia signalling represents a major genomic maintenance pathway that is activated in response to replication stress, impinging on stalled replication fork stability and recovery. Here, we report that upon replication stress, phosphorylation of the FANCD2 N-terminus by CHK1 triggers FBXL12-dependent proteasomal degradation of FANCD2, facilitating clearance of FANCD2 at stalled replication forks. This mechanism is required to promote efficient and faithful DNA replication under conditions of CYCLIN E- and drug-induced replication stress. Notably, reconstitution of FANCD2 with mutations in the N-terminal phosphodegron fail to re-establish fork progression in FANCD2-deficient human fibroblasts in response to replication stress. In the absence of FBXL12, FANCD2 becomes trapped on chromatin leading to replication stress, excessive DNA damage, and cell death. In human cancers, FBXL12, CYCLIN E, and Fanconi anaemia signalling are positively correlated and upregulation or amplification of FBXL12 is linked to reduced survival in patients with high CYCLIN E expressing breast tumours. Finally, depletion of FBXL12 exacerbated oncogene-induced replication stress and sensitised breast cancer cells to drug-induced replication stress by WEE1 inhibition. Collectively, our results indicate that FBXL12 constitutes a vulnerability of CYCLIN E-overexpressing cancer cells and may represent a novel target for cancer therapy.

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Chromatin immunopreciptiation of human lymphoblastoid cells to identify histone H3K9/14 acetylation regions at common fragile sites

Project description:Map the histone H3K9/14 acetylation regions of in human cells at 7 common fragile sites and their flanking non-fragile sequences as well as a 200kb containing the rare fragile site FRAXA, a 1,075kb non-fragile region on chr22, a hyperacetylated region HALPHA44, and a heterochromatic region HET405. The acetylated regions were mapped in untreated, aphidicolin(APH)-treated, trichostatin(TSA)-treated, and TSA plus APH-treated cells by combining the chromatin-immunoprecipitation with a tiled microarray platform (ChIP-chip).

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Hematopoiesis in Murine Fancd2-/- vs WT Fetal Liver

Project description:Hematopoiesis in Murine Fancd2-/- vs WT Fetal Liver

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