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P300/CBP mediated activation of MHCI machinery and IFNg receptor loci controls chemoimmunotherapy

ABSTRACT: p300/CBP mediated activation of MHCI machinery and IFNg receptor loci controls chemoimmunotherapy

PROVIDER: PRJNA636609 | ENA |

REPOSITORIES: ENA

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p300/CBP mediated activation of MHCI machinery and IFNg receptor loci controls chemoimmunotherapy

Project description:Certain chemotherapeutic drugs potentiate responses to immune checkpoint inhibitors (ICI), including PD-(L)1 antibodies, but the mechanisms underlying this synergism are poorly understood. Many cancers evade immune rejection by suppressing MHC-I antigen processing and presentation (AgPP). We show that two classes of DNA damaging drugs, platinoids (e.g. oxaliplatin) and topoisomerase inhibitors (e.g. mitoxanthrone), induce NF-kB activation, nuclear translocation of the histone and lysine acetyl transferases p300/CBP, interferon (IFN) regulatory factors and IFNg receptor 2 (IFNgR2). This results in transcriptional activation of loci coding for the MHC-I transactivator NLRC5 and components of the MHC-I AgPP machinery. Accordingly, p300 inactivation prevents drug-induced upregulation of MHC-I antigen presentation leading to impaired recognition of cancer cells by effector CD8+ T cells, whose tumor rejecting activity is IFNgR2-dependent. Correspondingly, EP300 loss in human cancers correlates with reduced expression of MHC-I related genes and/or changes in neoantigen amount and expression, suggesting that p300 is an immune-directed oncosuppressor.

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Project description:Histone acetylation is important for the activation of gene transcription but little is known about its direct ‘read/write’ mechanisms. Here, we report cryo-electron microscopy structures in which a p300/CBP multidomain monomer recognizes histone H4 N-terminal tail (NT) acetylation (ac) in a nucleosome and acetylates non-H4 histone NTs within the same nucleosome. p300/CBP not only recognized H4NTac via the bromodomain pocket responsible for ‘reading’, but also interacted with the DNA minor grooves via the outside of that pocket. This directed the catalytic center of p300/CBP to one of the non-H4 histone NTs. The primary target that p300 ‘writes’ by ‘reading’ H4NTac was H2BNT, and H2BNTac promoted H2A-H2B dissociation from the nucleosome. We propose a model in which p300/CBP ‘replicates’ histone NT acetylation within the H3-H4 tetramer to inherit epigenetic storage, and ‘transcribes’ it from the H3-H4 tetramer to the H2B-H2A dimers to activate context-dependent gene transcription through local nucleosome destabilization.

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