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KLF3 Mediates Epidermal Differentiation through the Epigenomic Writer CBP
Jackson Jones1, Yifang Chen1, Manisha Tiwari1
1Department of Dermatology, Department of Cellular and Molecular Medicine, UCSD Stem Cell Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0869, USA.
Iscience
|July 14, 2020
Summary
Transcription factor KLF3 is crucial for skin cell differentiation. It recruits CBP to activate enhancers, promoting epidermal differentiation and preventing skin diseases.
Area of Science:
- Cell Biology
- Molecular Biology
- Dermatology
Background:
- Skin diseases affect approximately 20% of the population, often stemming from impaired epidermal differentiation.
- Understanding the molecular mechanisms regulating epidermal differentiation is critical for addressing these conditions.
Purpose of the Study:
- To identify key regulators of epidermal differentiation.
- To elucidate the role of the transcription factor KLF3 in this process.
Main Methods:
- Investigated KLF3's function through gene knockdown experiments.
- Analyzed KLF3's genomic binding sites and its co-localization with CBP (a histone acetyltransferase).
- Assessed the impact of KLF3 depletion on enhancer activity and gene expression.
Main Results:
- KLF3 knockdown reduced differentiation gene expression and increased cell cycle gene expression.
- KLF3 primarily binds to active enhancers near differentiation-dependent genes.
- KLF3 depletion led to decreased CBP recruitment to enhancers, impairing enhancer activation.
Conclusions:
- KLF3 acts as a critical regulator of epidermal differentiation.
- KLF3 is essential for recruiting CBP to activate enhancers, thereby driving differentiation gene expression.
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