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DDR IN LYMPHOCYTES

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Cerrado

Identifying Functional Proteins at DNA Breaks with Quantitative Proteomics in Pr...

Identifying Functional Proteins at DNA Breaks with Quantitative Proteomics in Primary Lymphocytes DNA double-strand breaks (DSBs) in our genome that are not repaired properly can lead to various developmental, immunological, and neurological disorders and are a major driver for genomic instability and tumorigenesis. The role o... ver más

31/03/2016

UCPH

231K€

Presupuesto del proyecto: 231K€

Líder del proyecto

KOBENHAVNS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2016-03-31 No tenemos la información de la convocatoria

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1 Participantes

UCPH

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Líder del proyecto

KOBENHAVNS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 231K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto DNA double-strand breaks (DSBs) in our genome that are not repaired properly can lead to various developmental, immunological, and neurological disorders and are a major driver for genomic instability and tumorigenesis. The role of chromatin accessibility is of key importance to understand how the DNA/chromatin template senses and amplifies the DNA damage signal to properly repair the DNA in its native context. While all cells employ mechanisms for repairing DSBs, lymphocytes have uniquely adapted the same repair pathways for generating antibody diversity. During an immune response, B-lymphocytes undergo physiological DNA damage initiated by the activated-induced cytidine deaminase (AID) in a DNA rearrangement reaction called immunoglobulin heavy-chain (IgH) class-switch recombination (CSR). If AID-induced DNA breaks are not properly resolved, this B cell-specific DNA damage can lead to the formation of oncogenic chromosomal translocations; however, it is poorly understood how chromatin-associated factors coordinate this recombination reaction to suppress genomic instability. Here, I propose to use a novel approach combining chromatin immunoprecipitation and mouse genetics with state-of-the-art mass spectrometry-based label-free quantitative proteomics to identify and elucidate chromatin-bound proteins at DSBs. I will define the protein landscapes at DSBs in response to both γ-IR- and AID-induced DNA damage, based on our preliminary data, with unprecedented resolution and statistical confidence. I will perform detailed functional characterization of a subset of proteins using complementary approaches that investigate the repair of IR- and AID-induced DNA damage in lymphocytes. These combined unbiased proteomic and focused cell-based studies will deepen our understanding of the role of chromatin in the DNA damage response and DSB repair and may provide relevant targets for rationale design of therapeutic strategies for cancer or immunodeficiency disease.

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