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Related Concept Videos

Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying DNA...
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The extent of chromatin compaction can be studied by staining chromatin using specific DNA binding dyes. Under the microscope, the dense-compacted regions that take up more dye are called heterochromatin. Heterochromatin is further classified into two forms – constitutive heterochromatin and facultative heterochromatin.
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Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Measuring Single-Cell Aging with an Imaging-based Biomarker of Chromatin and Epigenetic Aging
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Published on: January 30, 2026

A Persistent Homology Approach Enables Single-Cell Detection of Chromatin Spatial Organization Changes During

Kanji Furuya1, Yoshitaka Umeno2, Masae Ikura3

  • 1Laboratory of Genome Maintenance, Department of Genome Biology, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms
|June 16, 2026
PubMed
Summary

This study introduces persistent homology (PH) to analyze single-cell nuclear architecture. PH quantifies chromatin changes in pathological senescence, revealing links between DNA damage and global chromatin structure.

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Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Area of Science:

  • Cellular Biology
  • Genomics
  • Biophysics

Background:

  • Chromatin organization and higher-order chromosome architecture change with aging and senescence.
  • Existing methods for analyzing chromosome structure are limited to population-level data.
  • Single-cell analysis is crucial for understanding variations in chromatin states.

Purpose of the Study:

  • To develop and apply a single-cell approach for quantifying higher-order chromosome structure alterations.
  • To investigate chromatin reorganization during pathological senescence using topological data analysis.
  • To correlate local DNA damage patterns with global chromatin structure in individual cells.

Main Methods:

  • Application of persistent homology (PH), a topological data analysis framework.
  • Quantification of spatial features of γH2AX foci and DAPI-stained chromatin in single-cell fluorescence images.
  • Machine learning analysis of topological features extracted from a model of pathological senescence.

Main Results:

  • Unsupervised analysis identified spatial patterns in γH2AX and DAPI signals associated with pathological senescence.
  • Classifications based on γH2AX foci corresponded with DAPI-based chromatin organization, linking local DNA damage to global structure.
  • Supervised models successfully distinguished normal from pathological senescent cells, with DAPI features indicating nuclear intensity gradient contributions.

Conclusions:

  • Persistent homology enables quantitative, single-cell characterization of nuclear architecture.
  • This approach provides a framework for dissecting chromatin reorganization during cell state transitions.
  • Findings highlight the interplay between DNA damage and chromatin structure in cellular senescence.