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A Two-Step Strategy that Combines Epigenetic Modification and Biomechanical Cues to Generate Mammalian Pluripotent Cells
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p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming
Marta Martin-Lopez1, Laura Maeso-Alonso1, Sandra Fuertes-Alvarez1
1Instituto de Biomedicina (IBIOMED) and Departamento de Biología Molecular, University of León, University of Leon, Campus de Vegazana, Leon, Spain.
Cell Death & Disease
|September 8, 2017
Summary
The tumor suppressor p73 is essential for efficient cellular reprogramming into induced pluripotent stem cells (iPSCs). It enhances the mesenchymal-to-epithelial transition (MET) by activating the BMP pathway, crucial for iPSC generation.
Area of Science:
- Stem cell biology
- Molecular biology
- Cancer research
Background:
- Cellular reprogramming generates induced pluripotent stem cells (iPSCs) for disease modeling.
- Mesenchymal-to-epithelial transition (MET) is critical for fibroblast reprogramming into iPSCs.
- p53 inhibits MET, while p63 promotes it; p73's role is unclear.
Purpose of the Study:
- Investigate the role of p73 in cellular reprogramming.
- Determine p73's impact on the MET and iPSC generation.
- Elucidate the molecular mechanisms by which p73 influences reprogramming.
Main Methods:
- Derived total Trp73 knockout mouse embryonic fibroblasts, with and without Trp53.
- Examined reprogramming capacity using Yamanaka factors.
- Analyzed MET, pluripotency marker expression, and BMP pathway activation.
Main Results:
- p73 is required for effective reprogramming, even without p53.
- p73 deficiency impairs MET, leading to defects in iPSC maturation and epithelial phenotype.
- p73 enhances BMP pathway activation by repressing Smad6 promoter via DNp73.
Conclusions:
- p73 acts as a crucial enhancer of MET during cellular reprogramming.
- p73 promotes iPSC generation by positively modulating the BMP signaling pathway.
- Findings provide mechanistic insights into MET and identify p73 as a key regulator.
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