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32a1b43f-aba4-4d4d-a192-aa35f32e6ebd - samples

ABSTRACT: ChIP-Seq targeting the major cohesin core subunit RAD21 to represent cohesin occupancy and binding sites in cohesin-mutated (STA2 or RAD21 mutations) and wildtpye adult AMLs.

PROVIDER: EGAD00001011199 | EGA |

REPOSITORIES: EGA

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Expression data from Rad21 knock-down in ES cells

Project description:The Cohesin complex has recently been described to regulate gene expression. We wanted to determine the gene expression profile specific in mouse ES cells after depletion of the Cohesin subunit Rad21. We used microarrays to detail the global programme of gene expression underlying depletion of Rad21 and identified distinct early development related genes up-regulated and many pluripotency related genes downregulated. Rad21 was depleted in R1/E ES cells for 48h using esiRNAs against Rad21. An esiRNA against non-targeting Luciferase was used as a negative control

2011-05-19 | E-GEOD-23923 | biostudies-arrayexpress

Cohesin maintains replication timing to suppress DNA damage on cancer genes [PEM-seq: RAD21-shRNA]

Project description:Cohesin loss-of-function mutations are frequently observed in tumors, but the mechanism is unclear. Here, we found that depletion of RAD21, a core subunit of cohesin, leads to massive genome-wide DNA breaks, up to five-fold, and 147 translocation hotspot genes that are co-mutated with cohesin in multiple cancers. Increased DNA damages are independent of RAD21-loss-induced transcription alteration and loop anchor elimination. However, damage-induced chromosomal translocations coincide with the asymmetrically distributed Okazaki fragments of DNA replication, suggesting that RAD21 depletion causes replication stresses evidenced by the slower replication speed and increased stalled forks. Mechanistically, approximately 30% of the human genome exhibits an earlier replication timing after RAD21 depletion, caused by the early initiation of >900 extra dormant origins. Correspondingly, most translocation hotspot genes lie in timing-altered regions. Therefore, we conclude that cohesin dysfunction causes replication stresses induced by excessive DNA replication initiation, resulting in gross DNA damages that may promote tumorigenesis.

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Cohesin maintains replication timing to suppress DNA damage on cancer genes [HU120-CBE_NAIL-seq_END-seq]

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Perturbation on DNA replication by cohesin dysfunction leads to gross genomic damages [END-seq]

Project description:Cohesin loss-of-function mutations are frequently observed in tumors, but the mechanism is unclear. Here, we found that depletion of RAD21, a core subunit of cohesin, leads to massive DNA breaks, up to five-fold, and 147 translocation hotspot genes that are co-mutated with cohesin in multiple cancers. DNA damages are independent of RAD21-loss-induced transcription alteration and loop anchor elimination. However, translocation junctions coincide with the asymmetrically distributed Okazaki fragments of DNA replication, suggesting that RAD21 depletion causes replication stresses evidenced by the slower replication speed and increased stalled forks. Mechanistically, approximately 30% of the human genome exhibits an earlier replication timing after RAD21 depletion, caused by the early initiation of >900 extra dormant origins. Correspondingly, most translocation hotspot genes lie in timing-altered regions. Therefore, we conclude that cohesin dysfunction causes severe replication stresses induced by extra DNA replication, resulting in gross DNA damages that may induce tumorigenesis.

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