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Updated: Feb 9, 2026

Fate Mapping of Human Embryonic Stem Cells by Teratoma Formation
Published on: August 1, 2010
Interaction of p53 and ASPPs regulates rhesus monkey embryonic stem cells conversion to neural fate concomitant with
Shuang Wang1,2, Lichuan Yang3,4, Raoxian Bai1,2
1a Yunnan Key Laboratory of Primate Biomedicine Research, Institute of Primate Translational Medicine , Kunming University of Science and Technology , Kunming , China.
Abstract:
The tumor suppressor p53 is a key regulator of cell apoptosis and cell cycle arrest. Recent studies show that the delicate balance of p53 expression is important for neural tube defects, neuronal degeneration, embryonic lethality, as well as differentiation and dedifferentiation. Moreover, p53 showed different regulatory patterns between rodent and primate embryonic stem cells (ESCs). However, the role of p53 and apoptosis stimulating protein of p53 (ASPP) during neural differentiation (ND) from primate ESCs is still unknown. In this study, using an FGF-2 and/or HGF selectively containing ND culture systems for rhesus monkey ESCs (rESCs), the changes of p53 and ASPPs, and p53 targets, i.e. BAX and p21, were analyzed. Our results showed that the expression patterns of ASPP1/ASPP2 and iASPP were opposite in rESCs but similar in differentiated cells, and the expression of p53 was approximately consistent with BAX, but not p21. These findings indicate that the strong expression of iASPP in ESCs and weak expression of ASPP1/ASPP2 maintain the stability of stemness; and in ND niche, unimpaired iASPP may decrease its inhibition of ASPP1/ASPP2 expression, the interaction of p53 and ASPPs causing rESCs to convert towards a neural fate concomitant with apoptosis, but not to cell cycle arrest.
Insights
The tumor suppressor p53 and its related ASPP proteins play crucial roles in primate neural differentiation. Their expression patterns in rhesus monkey embryonic stem cells influence stemness stability and neural fate conversion with apoptosis.
Area of Science:
- Stem cell biology
- Developmental biology
- Molecular oncology
Background:
- The tumor suppressor p53 is vital for cell apoptosis and cell cycle arrest.
- p53 dysregulation is implicated in neural tube defects, neurodegeneration, and embryonic lethality.
- p53 exhibits distinct regulatory patterns in rodent versus primate embryonic stem cells (ESCs).
Purpose of the Study:
- To investigate the roles of p53 and apoptosis stimulating protein of p53 (ASPP) family members during neural differentiation (ND) of primate ESCs.
- To analyze the expression patterns of p53, ASPP1, ASPP2, iASPP, and p53 targets (BAX, p21) in rhesus monkey ESCs (rESCs) undergoing ND.
Main Methods:
- Utilized FGF-2 and/or HGF selectively containing ND culture systems for rhesus monkey ESCs (rESCs).
- Analyzed the expression levels of p53, ASPP family members (ASPP1, ASPP2, iASPP), and p53 target genes (BAX, p21).
Main Results:
- ASPP1/ASPP2 and iASPP showed opposite expression in rESCs but similar patterns in differentiated cells.
- p53 expression correlated with BAX expression but not with p21 expression during ND.
- High iASPP and low ASPP1/ASPP2 expression in ESCs maintained stemness stability.
Conclusions:
- The interaction between p53 and ASPPs promotes neural fate conversion and apoptosis in rESCs within the ND niche.
- Unimpaired iASPP may reduce its inhibition on ASPP1/ASPP2 during neural differentiation.
- These findings highlight a mechanism for primate ESCs differentiating into neural cells involving p53 and ASPPs, leading to apoptosis rather than cell cycle arrest.
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