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Replicative Cell Senescence

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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...

Replicative Cell Senescence

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Related Experiment Video

Updated: May 13, 2026

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

FOXA1 mediates p16(INK4a) activation during cellular senescence.

Qian Li¹, Yu Zhang, Jingxuan Fu

¹Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, China.

The EMBO Journal

|February 28, 2013

Summary

Forkhead box A1 protein (FOXA1) activates p16INK4a transcription during cellular senescence. It reduces nucleosome density, counteracts Polycomb repression, and interacts with a distal enhancer to control p16INK4a expression.

More Related Videos

Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Related Experiment Videos

Last Updated: May 13, 2026

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Area of Science:

Molecular Biology
Cell Biology
Epigenetics

Background:

p16INK4a is a key regulator of cellular senescence.
Chromatin dynamics at the p16INK4a locus, particularly its promoter and enhancer, are not fully understood.

Purpose of the Study:

To investigate the role of Forkhead box A1 protein (FOXA1) in regulating p16INK4a transcription during cellular senescence.
To elucidate the mechanisms by which FOXA1 controls p16INK4a expression.

Main Methods:

Analysis of FOXA1 and p16INK4a expression in senescent cells.
Chromatin immunoprecipitation (ChIP) assays to assess FOXA1 binding and nucleosome density.
Investigation of Polycomb group protein interactions.
Identification and characterization of distal regulatory elements using genomic surveys and looping assays.

Main Results:

FOXA1 is upregulated in both replicative and oncogene-induced senescence.
FOXA1 acts as a transcriptional activator of p16INK4a, decreases nucleosome density at the promoter, and antagonizes Polycomb repression.
A distal enhancer element, approximately 150 kb away, interacts with the p16INK4a promoter to enhance its expression.

Conclusions:

FOXA1 plays a critical role in activating p16INK4a transcription during senescence through multiple mechanisms.
These mechanisms include direct transcriptional activation, modulation of chromatin accessibility, and antagonism of Polycomb silencing.
Long-range chromatin looping involving a distal enhancer contributes to FOXA1-mediated p16INK4a regulation.