Related Experiment Video
Updated: Jul 30, 2025
12:12
In vivo Reprogramming of Adult Somatic Cells to Pluripotency by Overexpression of Yamanaka Factors
Published on: December 17, 2013
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The E1a Adenoviral Gene Upregulates the Yamanaka Factors to Induce Partial Cellular Reprogramming
Gracia Mendoza1,2, Rebeca González-Pastor1,3, Juan Miguel Sánchez4
1Instituto Aragonés de Ciencias de la Salud (IACS), 50009 Zaragoza, Spain.
Cells
|May 13, 2023
Summary
Single gene expression can partially reprogram somatic cells. Adenoviral E1a-12S gene overexpression in mouse cells induced pluripotency-like traits, activating key gene networks.
Area of Science:
- Cell Biology
- Molecular Biology
- Epigenetics
Background:
- Induced pluripotent stem cells (iPSCs) are generated using reprogramming technologies, often involving multiple transcription factors.
- Adenoviral E1a gene has been shown to influence expression of reprogramming factors like c-Myc and Oct-4 and induce epigenetic alterations.
Purpose of the Study:
- To investigate if a single factor, specifically the adenoviral E1a-12S gene, is sufficient for partial cellular reprogramming.
- To explore the mechanism by which E1a-12S induces pluripotency-like characteristics.
Main Methods:
- Overexpression of the E1a-12S gene in mouse embryonic fibroblasts (MEFs).
- Analysis of pluripotency gene regulatory network activation.
- Assessment of induced pluripotent-like characteristics.
Main Results:
- E1a-12S overexpression alone was sufficient to induce pluripotent-like characteristics in MEFs.
- The reprogramming process involved the activation of the pluripotency gene regulatory network.
- The observed characteristics closely resembled those of epiblast stem cells.
Conclusions:
- A single factor (E1a-12S) can achieve partial reprogramming of somatic cells.
- This provides a potential mechanism linking viral infections to neoplasia through cellular reprogramming in specific microenvironments.
- Findings contribute to understanding the minimal requirements for cellular reprogramming and its implications in viral oncogenesis.
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