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The transcriptional response to oxidative stress

Project description

Dynamic remodelling of transcription upon oxidative stress

Oxidative stress is an imbalance between reactive oxygen species (free radicals) and the antioxidants that counteract them. In humans, it plays an essential role in cardiovascular and neurodegenerative diseases, cancer and diabetes. All organisms have an adaptive response to oxidative stress, typically the activation of so-called stress genes. A brief exposure to oxidative stress also leads to a rapid and transient global repression of transcription, but the molecular mechanism underlying this response is unknown. Funded by the European Research Council, the TranscriptStress project will investigate the transcriptome-wide oxidative stress response in human cells and in mice. State-of-the art sequencing, time-resolved proteomics and a novel screening approach should help fill this important knowledge gap.

Objective

Environmental stress triggers a cellular response to promote adaptation and survival, typically through activation of stress genes. What is less appreciated is that various types of cellular stress at the same time induce widespread transcriptional repression at most other genes. Although such transcriptional reprogramming is common to various kinds of cellular stress, recent evidence suggests it is governed by different stress-specific mechanisms. A brief exposure to oxidative stress leads to a rapid and transient global repression of transcription. However, our current knowledge about the oxidative stress response is extremely limited. Based on our preliminary results, I hypothesise that the transcriptional response to oxidative stress involves both regulation of transcription elongation as well as termination and that these are connected to post-translational modifications of RNA polymerase II (RNAPII) itself.

Here, I propose an ambitious approach to investigate the transcriptome-wide oxidative stress response in human cells and following physiologically induced oxidative stress in mice. To this end, we will use a combination of state-of-the art sequencing techniques coupled with time-resolved proteomics and a novel screening approach. Together, our work will provide important new knowledge about the transcriptional response to oxidative stress and the factors involved – in an area that is currently not well understood. Such knowledge is also crucial to understand the fundamental mechanisms allowing RNAPII to stop transcribing and restart again. Finally, we will investigate how factors involved in the transcriptional response influence transcription-associated genome instability and neuronal cell identity. This will be relevant for diseases in which oxidative stress has been implicated, such as neurological disorders and cancer.

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HORIZON-ERC - HORIZON ERC Grants

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Call for proposal

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(opens in new window) ERC-2022-STG

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Host institution

KOBENHAVNS UNIVERSITET
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 500 000,00
Address
NORREGADE 10
1165 KOBENHAVN
Denmark

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Region
Danmark Hovedstaden Byen København
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 1 500 000,00

Beneficiaries (1)

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