MassIVE MSV000089246

Partial Public PXD033182

A natural variation-based screen in mouse cells reveals USF2 as a regulator of DNA damage response and senescence

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Description

Mammalian cells of many types, upon exposure to stress, enter the senescence program. They stop dividing, become refractory to apoptosis, and release soluble inflammation and tissue remodeling factors referred to as the senescence-associated secretory phenotype (SASP). The resulting immune response, on an acute timescale, can clear debris, promote wound healing, and/or suppress tumorigenesis. However, during aging, senescent cells remain in the body long past any initial triggering event, resulting in chronic inflammation that damages the surrounding tissue. Landmark work has revealed the benefits of eliminating senescent cells, in terms of age-related pathologies and lifespan itself. We set out to develop a novel approach to survey transcription factors for a role in cellular senescence, with the potential for increased specificity relative to traditional genomic screens. Our strategy took advantage of the natural genetic variation in senescence gene expression, and transcription factor binding sites, across mouse species. Among the top hits from this analysis, we chose the under-studied factor USF2 for validation experiments, focused on gene regulation and cellular phenotypes during senescence induction and maintenance. [doi:10.25345/C5NC5SG97] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: DIA-MS, senescence, transcription factors, quantitative proteomics

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Principal Investigators:
(in alphabetical order) 		Birgit Schilling, Buck Institute, USA
Submitting User: cking
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