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Opposing chromatin remodeler activities control initiation frequency and start site selection

ABSTRACT: Opposing chromatin remodeler activities control initiation frequency and start site selection

PROVIDER: PRJNA474909 | ENA |

REPOSITORIES: ENA

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Opposing chromatin remodeler activities control initiation frequency and start site selection

Project description:Using an integrated analysis of chromatin remodeler binding in unperturbed cells and nucleosome displacement activity upon rapid remodeler depletion or degradation, we investigate the interplay between these enzymes and their functional consequences. We show that many promoters are acted upon by multiple remodelers that operate either cooperatively or in opposition to determine the precise location of the key transcription start site-associated +1 nucleosome. Functional assays indicate that +1 nucleosome positioning reflects a trade-off between maximizing RNA Polymerase II recruitment and minimizing transcription initiation at incorrect sites. Interestingly, in the absence of any remodeling activity +1 nucleosomes largely maintain their positions. Our results provide a detailed picture of fundamental mechanisms linking promoter nucleosome architecture to productive transcription initiation.

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Project description:Despite the emerging evidence of ferroptosis implicated in diverse pathological scenarios, molecular adaptors linking its oxidative inducers and chromatin as carrier of stable epigenetic memory for its propagation remain elusive. Here, we report the identification of two WD40 proteins DCAF8 and WDR76 as substrate adaptor and molecular inhibitor respectively of the Cullin-4 RING ubiquitin ligase (CRL4) system for stability control of the chromatin remodeler LSH. Degradation analysis and CRL4-DCAF8 complex reconstitution demonstrate that CRL4DCAF8 is a bona fide E3 ligase for LSH. In contrast, WDR76 antagonizes DCAF8-targeted LSH proteolysis through competitive inhibition of the holo-CRL4DCAF8-LSH complex assembly. Importantly, this opposing regulatory strategy is utilized in lipid hydroperoxide induced ferroptosis, and we identify key redox homeostasis genes significantly regulated by the DCAF8/WDR76/LSH axis through transcriptomic epistasis analysis. Such responsiveness could be attributed to increased ratio of DCAF8 over WDR76 for antagonistic LSH association accompanying ROS overproduction invoked decrease of TET-catalyzed DNA oxidation. Evaluation of epigenetic dynamics at DCAF8/WDR76/LSH-regulated gene promoters reveals linker histone H1- and LSH-associated transcriptional repression is coordinately removed in ferroptosis. Together with phenotypes driven by WDR76 and DCAF8 manipulations, these data identify DCAF8- and WDR76-governed LSH degradation as a crucial node in ferroptosis, tumorigenesis and senescence.

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