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Topoisomerase 1 facilitates nucleosome reassembly at stress genes during recovery [RNA-seq]

ABSTRACT: Investigate the role of topoisomerase 1 in the response to oxidative stress

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE227183 | GEO | 2023/10/23

REPOSITORIES: GEO

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Topoisomerase 1 facilitates nucleosome reassembly at stress genes during recovery [Mnase-seq]

Project description:Investigate the role of topoisomerase 1 in the response to oxidative stress

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Topoisomerase 1 facilitates nucleosome reassembly at stress genes during recovery.

Project description:Topoisomerase 1 facilitates nucleosome reassembly at stress genes during recovery.

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Topoisomerase 1 facilitates nucleosome reassembly at stress genes during recovery.

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

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Topoisomerase I Poisoning by Electrophiles Derived from Oxidative Stress

Project description:The cancer target enyzme topoisomerase 1 transiently cleaves one strand of chromosomal DNA to relax accumulated strain that can prevent transcription, replication or chromatin assembly. The topoisomerase 1 poison camptothecin and its synthetic analogs are widely used chemotherapeutics that act by trapping the enzyme on DNA in a ‘covalent complex’, resulting in persistent DNA damage and cell death. The prevailing model, interfacial inhibition, contends that the covalent complex is trapped by drug binding alone. In contrast, here we show that camptothecins produce extensive oxidative stress and that topoisomerase 1 is reactive with electrophilic second messengers of oxidative damage. We show that blocking oxidative stress in cells inhibits covalent complex formation by camptothecin, while electrophiles such as 4-hydroxynonenal are able to induce covalent complex formation in cells on their own. Towards mechanism of action, we show that 4-hydroxynonenal electrophilically modifies a cysteine within the DNA-binding active site of human topoisomerase 1. Taken together, our results suggest a mechanism in which oxidative stress mediates the effects of many topoisomerase 1 poisons, and suggest that this critical DNA-regulating enzyme may have a dual role as a sensor of cellular redox stress, linking oxidative stress to DNA damage response in cancer cells.

2021-03-24 | PXD018549 | Pride

Co-ordinate inhibiton of autism candidate genes by topoisomerase inhibitors [array]

Project description:Topoisomerases are necessary for the expression of neurodevelopmental genes, and are mutated in some patients with autism spectrum disorder (ASD). We have studied the effects of inhibitors of Topoisomerase 1 (Top1) and Topoisomerase 2 (Top2) enzymes on mouse cortical neurons. We find that topoisomerases selectively inhibit long genes (>100kb), with little effect on all other gene expression. Using ChIPseq against RNA Polymerase II (Pol2) we show that the Top1 inhibitor topotecan blocks transcriptional elongation of long genes specifically. Many of the genes inhibited by topotecan are candidate ASD genes, leading us to propose that topoisomerase inhibition might contribute to ASD pathology.

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Codependency of H2B monoubiquitination and nucleosome reassembly on Chd1.

Project description:Monoubiquitination of histone H2B on Lys 123 (H2BK123ub) is a transient histone modification considered to be essential for establishing H3K4 and H3K79 trimethylation by Set1/COMPASS and Dot1, respectively. Here, we identified Chd1 as a factor that is required for the maintenance of high levels of H2B monoubiquitination, but not for H3K4 and H3K79 trimethylation. Loss of Chd1 results in a substantial loss of H2BK123ub levels with little to no effect on the genome-wide pattern of H3K4 and H3K79 trimethylation. Our data show that nucleosomal occupancy is reduced in gene bodies in both chd1Δ and, as has been shown, K123A mutant backgrounds. We also demonstrated that Chd1's function in maintaining H2BK123ub levels is conserved from yeast to humans. Our study provides evidence that only small levels of H2BK123ub are necessary for full levels of H3K4 and H3K79 trimethylation in vivo and points to a possible role for Chd1 in positively regulating gene expression through promoting nucleosome reassembly coupled with H2B monoubiquitination.

| S-EPMC3347789 | biostudies-literature

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