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Related Concept Videos

Epigenetic Regulation01:46

Epigenetic Regulation

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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
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Regulation of Expression Occurs at Multiple Steps02:24

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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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Gene expression is the process in which DNA directs the synthesis of functional products, that is, proteins. Cells can regulate gene expression at various stages. It allows organisms to generate different cell types and enables cells to adapt to internal and external factors.
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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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Related Experiment Video

Updated: Jan 24, 2026

Visualization of Gut Microbiota-host Interactions via Fluorescence In Situ Hybridization, Lectin Staining, and Imaging
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Microbiota Inhibit Epithelial Pathogen Adherence by Epigenetically Regulating C-Type Lectin Expression.

Vivienne Woo1, Emily M Eshleman1, Taylor Rice1

  • 1Division of Immunobiology and Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, United States.

Frontiers in Immunology
|May 29, 2019
PubMed
Summary
This summary is machine-generated.

Commensal bacteria reduce pathogen adherence by epigenetically downregulating a host cell receptor. This microbiota-driven mechanism enhances innate immunity against intestinal infections.

Keywords:
CLECHDACcitrobacterepigeneticintestine epithelial cellsmicrobiota

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Area of Science:

  • Microbiology
  • Immunology
  • Epigenetics

Background:

  • Bacterial pathogens adhere to intestinal epithelial cells for infection.
  • Commensal bacteria are known to protect against pathogens, but the mechanisms are unclear.
  • The role of the microbiota in modulating host cell pathways affecting pathogen adherence requires further investigation.

Purpose of the Study:

  • To investigate how the gut microbiota influences the adherence of bacterial pathogens to host epithelial cells.
  • To identify host cell factors and pathways regulated by the microbiota that impact pathogen binding.
  • To elucidate the epigenetic mechanisms by which the microbiota control host gene expression related to pathogen defense.

Main Methods:

  • Comparison of germ-free mice with conventionally colonized mice.
  • Analysis of epithelial cell surface glycoprotein expression, specifically C-type lectin 2e (Clec2e).
  • Functional studies involving Clec2e overexpression and assessment of pathogen adherence.
  • Investigation of histone acetylation/deacetylation at the Clec2e gene locus.
  • Assessment of histone deacetylase 3 (HDAC3) involvement in Clec2e regulation.

Main Results:

  • The gut microbiota significantly decreases bacterial pathogen adherence to intestinal epithelial cells.
  • Microbiota colonization leads to reduced expression of the C-type lectin 2e (Clec2e) on epithelial cells.
  • Overexpression of Clec2e enhances the adherence of intestinal bacterial pathogens.
  • Downregulation of Clec2e by the microbiota correlates with decreased histone acetylation of the Clec2e gene.
  • Histone deacetylase 3 (HDAC3) mediates the epigenetic silencing of Clec2e.

Conclusions:

  • Commensal bacteria epigenetically regulate host epithelial cells to reduce expression of Clec2e.
  • This microbiota-induced decrease in Clec2e limits pathogen adherence, enhancing innate defense.
  • The study reveals a novel mechanism involving epigenetic control by the microbiota in host-pathogen interactions.