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Article

H2B Type 1-K Accumulates in Senescent Fibroblasts with Persistent DNA Damage along with Methylated and Phosphorylated Forms of HMGA1

1
Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, 91190 Gif-sur-Yvette, France
2
Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA
3
Stanford Cardiovascular Institute, Stanford University, Stanford, CA 94305, USA
4
Département Médicaments et Technologies Pour la Santé (DMTS), Université Paris-Saclay, CEA, INRAE, MetaboHUB, 91191 Gif-sur-Yvette, France
*
Authors to whom correspondence should be addressed.
Proteomes 2021, 9(2), 30; https://doi.org/10.3390/proteomes9020030
Submission received: 21 May 2021 / Revised: 11 June 2021 / Accepted: 17 June 2021 / Published: 21 June 2021
(This article belongs to the Special Issue Latest Discoveries and Proteomics-Based Methods in Histone Biology)

Abstract

Cellular senescence is a state of terminal proliferative arrest that plays key roles in aging by preventing stem cell renewal and by inducing the expression of a series of inflammatory factors including many secreted proteins with paracrine effects. The in vivo identification of senescent cells is difficult due to the absence of universal biomarkers. Chromatin modifications are key aspects of the senescence transition and may provide novel biomarkers. We used a combined protein profiling and bottom-up mass spectrometry approach to characterize the isoforms and post-translational modifications of chromatin proteins over time in post-mitotic human fibroblasts in vitro. We show that the H2B type 1-K variant is specifically enriched in deep senescent cells with persistent DNA damage. This accumulation was not observed in quiescent cells or in cells induced into senescence without DNA damage by expression of the RAF kinase. Similarly, HMGA1a di-methylated and HMGA1b tri-phosphorylated forms accumulated exclusively in the chromatin of cells in deep senescent conditions with persistent DNA damage. H2B type 1-K and modified HMGA1 may thus represent novel biomarkers of senescent cells containing persistent DNA damage.
Keywords: histone variants; histone post-translational modifications; mass spectrometry; senescence; quiescence histone variants; histone post-translational modifications; mass spectrometry; senescence; quiescence
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MDPI and ACS Style

Contrepois, K.; Mann, C.; Fenaille, F. H2B Type 1-K Accumulates in Senescent Fibroblasts with Persistent DNA Damage along with Methylated and Phosphorylated Forms of HMGA1. Proteomes 2021, 9, 30. https://doi.org/10.3390/proteomes9020030

AMA Style

Contrepois K, Mann C, Fenaille F. H2B Type 1-K Accumulates in Senescent Fibroblasts with Persistent DNA Damage along with Methylated and Phosphorylated Forms of HMGA1. Proteomes. 2021; 9(2):30. https://doi.org/10.3390/proteomes9020030

Chicago/Turabian Style

Contrepois, Kévin, Carl Mann, and François Fenaille. 2021. "H2B Type 1-K Accumulates in Senescent Fibroblasts with Persistent DNA Damage along with Methylated and Phosphorylated Forms of HMGA1" Proteomes 9, no. 2: 30. https://doi.org/10.3390/proteomes9020030

APA Style

Contrepois, K., Mann, C., & Fenaille, F. (2021). H2B Type 1-K Accumulates in Senescent Fibroblasts with Persistent DNA Damage along with Methylated and Phosphorylated Forms of HMGA1. Proteomes, 9(2), 30. https://doi.org/10.3390/proteomes9020030

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