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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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Embryonic stem (ES) cells were first discovered in mice in 1981 by Martin Evans. In 1998, James Thomson identified a method to isolate embryonic stem cells from humans. Human embryonic stem cells (hESCs) are obtained from 3-5 day old embryos that remain unused after an in vitro fertilization procedure.
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Actl6a protects embryonic stem cells from differentiating into primitive endoderm.

Weisi Lu1,2,3, Lekun Fang4, Bin Ouyang5

  • 1Key Laboratory of Gene Engineering of the Ministry of Education, Institute of Healthy Aging Research and SYSU-BCM Joint Research Center, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.

Stem Cells (Dayton, Ohio)
|March 25, 2015
PubMed
Summary
This summary is machine-generated.

Actin-like protein 6A (Actl6a) prevents mouse embryonic stem cell differentiation into primitive endoderm. Its knockdown induces differentiation, while its expression represses it, revealing a novel gatekeeper role.

Keywords:
Actl6aEmbryonic stem cellsPrimitive endodermSelf-renewalTip60-p400 complex

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Area of Science:

  • Stem cell biology
  • Epigenetics
  • Developmental biology

Background:

  • Actin-like protein 6A (Actl6a) is a subunit of chromatin remodeling complexes essential for embryonic stem cell (ESC) maintenance.
  • The mechanisms governing epiblast (EPI) and primitive endoderm (PrE) specification from the inner cell mass (ICM) are not fully understood.

Purpose of the Study:

  • To investigate the function of Actl6a in mouse ESCs (mESCs) and its role in EPI/PrE specification.
  • To elucidate the molecular mechanisms by which Actl6a regulates mESC differentiation.

Main Methods:

  • RNA interference (RNAi) for Actl6a knockdown.
  • Ectopic expression of Actl6a.
  • Co-immunoprecipitation to assess protein interactions.
  • Chromatin immunoprecipitation to analyze gene promoter binding.
  • Quantitative real-time PCR for gene expression analysis.

Main Results:

  • Actl6a is highly expressed in mESCs and downregulated during differentiation.
  • Actl6a knockdown induced mESC differentiation towards the PrE lineage, while ectopic Actl6a repressed it.
  • Actl6a interacts with Nanog and Sox2, promoting Nanog binding to pluripotency genes.
  • Actl6a targets PrE regulator promoters (Sall4, Fgf4), repressing their expression.

Conclusions:

  • Actl6a functions as a novel gatekeeper in mESCs, preventing differentiation into the PrE lineage.
  • Actl6a's role involves interaction with key pluripotency factors and direct repression of PrE regulators.
  • These findings reveal a Yin/Yang regulatory pattern for Actl6a in maintaining mESC pluripotency.