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Related Concept Videos

Chromatin Modification in iPS Cells01:32

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
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The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
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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...
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In 1928, a German botanist Emil Heitz observed the moss nuclei with a DNA binding dye. He observed that while some chromatin regions decondense and spread out in the interphase nucleus, others do not. He termed them euchromatin and heterochromatin, respectively. He proposed that the heterochromatin regions reflect a functionally inactive state of the genome. It was later confirmed that heterochromatin is transcriptionally repressed, and euchromatin is transcriptionally active chromatin.
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CRISPR-Mediated Reorganization of Chromatin Loop Structure
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Disordered chromatin packing regulates phenotypic plasticity.

Ranya K A Virk1, Wenli Wu1, Luay M Almassalha1,2,3

  • 1Department of Biomedical Engineering, Northwestern University, Evanston, IL 60208, USA.

Science Advances
|January 15, 2020
PubMed
Summary
This summary is machine-generated.

Chromatin packing (CP) and macromolecular crowding (MC) influence gene expression and phenotypic plasticity. Physical factors, especially chromatin packing scaling, regulate cellular responses and are linked to cancer patient survival.

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Area of Science:

  • * Biophysics
  • * Molecular Biology
  • * Computational Biology

Background:

  • * Three-dimensional supranucleosomal chromatin packing significantly impacts gene expression.
  • * Gene accessibility, binding affinities, and molecular diffusion are key regulatory mechanisms.
  • * Physical factors within the cellular environment play a crucial role in gene regulation.

Purpose of the Study:

  • * To investigate how physical factors of chromatin packing and macromolecular crowding influence gene expression.
  • * To computationally model the interplay between disordered chromatin packing (CP) and local macromolecular crowding (MC).
  • * To identify the role of chromatin density, packing scaling, and domain size in gene expression regulation.

Main Methods:

  • * Development of a computational model integrating disordered chromatin packing (CP) and local macromolecular crowding (MC).
  • * Computational and experimental validation of model predictions.
  • * Application of the chromatin packing and macromolecular crowding (CPMC) model to cancer patient transcriptional data.

Main Results:

  • * Identified chromatin packing scaling as a critical factor in regulating phenotypic plasticity.
  • * Demonstrated that physical factors influence intercellular transcriptional malleability and heterogeneity, affecting stressor responsiveness.
  • * Found an inverse relationship between cancer patient survival and tumor cell phenotypic plasticity.

Conclusions:

  • * Physical properties of chromatin packing, particularly scaling, are major regulators of gene expression and phenotypic plasticity.
  • * The interplay of chromatin packing and macromolecular crowding impacts cellular responses to environmental stressors.
  • * Phenotypic plasticity in tumor cells, influenced by chromatin packing, correlates with patient survival outcomes.