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Updated: May 28, 2026

Chromatin Immunoprecipitation Assay for Tissue-specific Genes using Early-stage Mouse Embryos

Chromatin Immunoprecipitation Assay for Tissue-specific Genes using Early-stage Mouse Embryos

Published on: April 29, 2011

Deciphering c-MYC-regulated genes in two distinct tissues.

Samuel C Robson¹, Lesley Ward, Helen Brown

¹Wellcome Trust/Cancer Research UK Gurdon Institute, Cambridge, CB2 1QN, UK.

|October 4, 2011

Summary

This summary is machine-generated.

MYC activation drives cell growth and cycle entry in both skin and pancreatic cells. However, it triggers apoptosis in pancreatic cells while promoting survival and angiogenesis in skin cells, revealing distinct cellular responses to MYC.

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Area of Science:

Molecular Biology
Cell Biology
Oncology

Background:

The transcription factor MYC regulates crucial cellular processes like replication and apoptosis.
Understanding MYC-driven gene expression differences leading to opposing outcomes in vivo is essential.
This study investigates MYC's role in skin and pancreatic cells to elucidate these differences.

Purpose of the Study:

To examine time-dependent global gene expression changes following MYC activation in distinct cell types.
To identify the molecular mechanisms underlying differential cellular responses, including apoptosis and tissue expansion/involution.
To compare MYC-induced gene expression patterns in skin suprabasal keratinocytes and pancreatic islet β-cells.

Main Methods:

Utilized two transgenic mouse models with MYC activation in specific cell types.
Analyzed time-dependent global gene expression changes.
Correlated gene expression data with observed tissue phenotypes (expansion/involution).

Main Results:

MYC activation increased cell cycle, growth, and metabolism genes in both cell types, while down-regulating differentiation genes.
Pancreatic β-cells showed increased expression of DNA-damage and apoptotic genes (Atr, Arf, Bax, Cycs).
Skin keratinocytes exhibited down-regulated pro-apoptotic genes (Noxa), up-regulated anti-apoptotic pathways (Igf1-Akt), and induced angiogenesis, with Kallikrein family up-regulation.

Conclusions:

MYC activation induces cell growth, differentiation loss, and cell cycle entry in both β-cells and keratinocytes.
Apoptosis in β-cells involves DNA-damage response and pro-apoptotic pathways (Cdc2a, p19(Arf)/p53).
Apoptosis avoidance in keratinocytes is linked to anti-apoptotic pathways (Igf1-Akt), angiogenesis, and potential intrinsic resistance to p19(Arf) induction.