scholarly journals Erosion of the Epigenetic Landscape and Loss of Cellular Identity as a Cause of Aging in Mammals

2019 ◽  
Author(s):  
Jae-Hyun Yang ◽  
Patrick T. Griffin ◽  
Daniel L. Vera ◽  
John K. Apostolides ◽  
Motoshi Hayano ◽  
...  
Keyword(s):  
Epigenetic Landscape ◽  
Cellular Identity

scholarly journals Aberrant Epigenetic Landscape in Cancer: How Cellular Identity Goes Awry

2010 ◽  
Vol 19 (5) ◽  
pp. 698-711 ◽  
Author(s):  
María Berdasco ◽  
Manel Esteller
Keyword(s):  
Epigenetic Landscape ◽  
Cellular Identity

scholarly journals Erosion of the Epigenetic Landscape and Loss of Cellular Identity as a Cause of Aging in Mammals

2019 ◽  
Author(s):  
Jae-Hyun Yang ◽  
Patrick T. Griffin ◽  
Daniel L. Vera ◽  
John K. Apostolides ◽  
Motoshi Hayano ◽  
...  
Keyword(s):  
Yeast Cells ◽  
Epigenetic Landscape ◽  
Dna Breaks ◽  
Cell Identity ◽  
Epigenetic Information ◽  
Living Things ◽  
Yeast Aging ◽  
Tissue Changes ◽  
Cellular Identity ◽  
Over Time

SUMMARYAll living things experience entropy, manifested as a loss of inherited genetic and epigenetic information over time. As budding yeast cells age, epigenetic changes result in a loss of cell identity and sterility, both hallmarks of yeast aging. In mammals, epigenetic information is also lost over time, but what causes it to be lost and whether it is a cause or a consequence of aging is not known. Here we show that the transient induction of genomic instability, in the form of a low number of non-mutagenic DNA breaks, accelerates many of the chromatin and tissue changes seen during aging, including the erosion of the epigenetic landscape, a loss of cellular identity, advancement of the DNA methylation clock and cellular senescence. These data support a model in which a loss of epigenetic information is a cause of aging in mammals.One Sentence SummaryThe act of repairing DNA breaks induces chromatin reorganization and a loss of cell identity that may contribute to mammalian aging

Diabetes alters the epigenetic landscape of the oocyte and early embryo

2014 ◽  
Author(s):  
Hannah M Brown ◽  
Melissa A White ◽  
Laura A Frank ◽  
Jeremy G Thompson
Keyword(s):  
Early Embryo ◽  
Epigenetic Landscape

scholarly journals Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing

2021 ◽  
Vol 22 (9) ◽  
pp. 4959
Author(s):  
Lilas Courtot ◽  
Elodie Bournique ◽  
Chrystelle Maric ◽  
Laure Guitton-Sert ◽  
Miguel Madrid-Mencía ◽  
...  
Keyword(s):  
Replication Timing ◽  
Replication Stress ◽  
Chromatin Accessibility ◽  
Cell Type ◽  
Replicative Stress ◽  
Daughter Cells ◽  
Origin Activation ◽  
Cell Type Specific ◽  
Cellular Identity ◽  
Dna Replication Timing

DNA replication timing (RT), reflecting the temporal order of origin activation, is known as a robust and conserved cell-type specific process. Upon low replication stress, the slowing of replication forks induces well-documented RT delays associated to genetic instability, but it can also generate RT advances that are still uncharacterized. In order to characterize these advanced initiation events, we monitored the whole genome RT from six independent human cell lines treated with low doses of aphidicolin. We report that RT advances are cell-type-specific and involve large heterochromatin domains. Importantly, we found that some major late to early RT advances can be inherited by the unstressed next-cellular generation, which is a unique process that correlates with enhanced chromatin accessibility, as well as modified replication origin landscape and gene expression in daughter cells. Collectively, this work highlights how low replication stress may impact cellular identity by RT advances events at a subset of chromosomal domains.

Genome‐Wide DNA (hydroxy)methylation reveals the individual epigenetic landscape importance on osteogenic phenotype acquisition in periodontal ligament cells

2021 ◽  
Author(s):  
Rogério S. Ferreira ◽  
Rahyza I. F. Assis ◽  
Geórgia da S. Feltran ◽  
Iasmin Caroline do Rosário Palma ◽  
Beatriz G. Françoso ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Epigenetic Landscape ◽  
Genome Wide ◽  
The Individual

scholarly journals Reconstructing an epigenetic landscape using a genetic pulling approach

2021 ◽  
Vol 103 (6) ◽  
Author(s):  
Michael Assaf ◽  
Shay Be'er ◽  
Elijah Roberts
Keyword(s):  
Epigenetic Landscape

scholarly journals A generalization of t-SNE and UMAP to single-cell multimodal omics

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Van Hoan Do ◽  
Stefan Canzar
Keyword(s):  
Dimensionality Reduction ◽  
Single Cell ◽  
Cell Types ◽  
High Dimensional ◽  
Omics Data ◽  
Relative Contribution ◽  
Reduction Techniques ◽  
Dimensionality Reduction Techniques ◽  
Concise Representation ◽  
Cellular Identity

AbstractEmerging single-cell technologies profile multiple types of molecules within individual cells. A fundamental step in the analysis of the produced high-dimensional data is their visualization using dimensionality reduction techniques such as t-SNE and UMAP. We introduce j-SNE and j-UMAP as their natural generalizations to the joint visualization of multimodal omics data. Our approach automatically learns the relative contribution of each modality to a concise representation of cellular identity that promotes discriminative features but suppresses noise. On eight datasets, j-SNE and j-UMAP produce unified embeddings that better agree with known cell types and that harmonize RNA and protein velocity landscapes.

scholarly journals Targeting DNA Methylation Depletes Uterine Leiomyoma Stem Cell–enriched Population by Stimulating Their Differentiation

Endocrinology ◽  
2020 ◽  
Vol 161 (10) ◽  
Author(s):  
Shimeng Liu ◽  
Ping Yin ◽  
Jingting Xu ◽  
Ariel J Dotts ◽  
Stacy A Kujawa ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Stem Cell ◽  
Cell Population ◽  
Uterine Leiomyoma ◽  
Stem Cell Population ◽  
Epigenetic Landscape ◽  
Stem Cell Regulation ◽  
Integrative Analyses ◽  
Associated Functions ◽  
Intermediate Cells

Abstract Uterine leiomyoma (LM) is the most common tumor in women and can cause severe morbidity. Leiomyoma growth requires the maintenance and proliferation of a stem cell population. Dysregulated deoxyribonucleic acid (DNA) methylation has been reported in LM, but its role in LM stem cell regulation remains unclear. Here, we fluorescence-activated cell sorting (FACS)-sorted cells from human LM tissues into 3 populations: LM stem cell–like cells (LSC, 5%), LM intermediate cells (LIC, 7%), and differentiated LM cells (LDC, 88%), and we analyzed the transcriptome and epigenetic landscape of LM cells at different differentiation stages. Leiomyoma stem cell–like cells harbored a unique methylome, with 8862 differentially methylated regions compared to LIC and 9444 compared to LDC, most of which were hypermethylated. Consistent with global hypermethylation, transcript levels of TET1 and TET3 methylcytosine dioxygenases were lower in LSC. Integrative analyses revealed an inverse relationship between methylation and gene expression changes during LSC differentiation. In LSC, hypermethylation suppressed the genes important for myometrium- and LM-associated functions, including muscle contraction and hormone action, to maintain stemness. The hypomethylating drug, 5′-Aza, stimulated LSC differentiation, depleting the stem cell population and inhibiting tumor initiation. Our data suggest that DNA methylation maintains the pool of LSC, which is critical for the regeneration of LM tumors.

Cellular identity and lineage choice

2002 ◽  
Vol 2 (12) ◽  
pp. 977-982 ◽  
Author(s):  
Amanda G. Fisher
Keyword(s):  
Cellular Identity
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