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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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Directed Differentiation of Hemogenic Endothelial Cells from Human Pluripotent Stem Cells
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CHD7 regulates definitive endodermal and mesodermal development from human embryonic stem cells.

Rong Hu1, Jin Zhao1, Kuan Chen Lai1

  • 1Department of Allied Health Sciences, University of Connecticut, 1390 Storrs Road, Storrs, 06269, CT, USA.

Stem Cell Research & Therapy
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CHD7 gene deletion impairs human embryonic stem cell development into definitive endoderm and mesoderm. This reveals CHD7

Keywords:
CHARGE syndromeCHD7Definitive endodermHuman embryonic stem cells

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Area of Science:

  • Developmental Biology
  • Genetics
  • Stem Cell Research

Background:

  • CHD7 mutations cause developmental disorders like CHARGE syndrome, but mechanisms are unclear.
  • Embryonic definitive endoderm (DE) is crucial for forming vital organs.
  • Understanding CHD7's role in early development is essential.

Purpose of the Study:

  • To investigate the role of CHD7 in human embryonic stem cell (hESC) differentiation.
  • To determine how CHD7 deletion affects the development of definitive endoderm (DE) and mesoderm.
  • To explore the molecular mechanisms underlying CHD7-related developmental defects.

Main Methods:

  • Generated CHD7 mutant (CHD7-/- and CHD7+/-) and wild-type (CHD7+/+) hESCs using CRISPR/Cas9.
  • Assessed hESC differentiation into DE, mesoderm, and ectoderm in vitro.
  • Performed RNA sequencing (RNA-seq) and ATAC-seq to compare gene expression and chromatin accessibility.

Main Results:

  • CHD7 deletion reduced hESC differentiation into DE and mesoderm in a dose-dependent manner.
  • Significant alterations in gene expression and chromatin accessibility were observed in CHD7-deleted cells.
  • Identified 40 genes with decreased expression and accessibility in CHD7-deleted hESC-DE cells.

Conclusions:

  • CHD7 is essential for DE and mesodermal development from hESCs.
  • Provides novel insights into how CHD7 mutations lead to congenital anomalies.
  • Highlights CHD7's critical function in early human development.