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Related Concept Videos

Determination01:51

Determination

During embryogenesis, cells become progressively committed to different fates through a two-step process: specification followed by determination. Specification is demonstrated by removing a segment of an early embryo, “neutrally” culturing the tissue in vitro—for example, in a petri dish with simple medium—and then observing the derivatives. If the cultured region gives rise to cell types that it would normally generate in the embryo, this means that it is specified. In contrast, determination...
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Multipotency of Hematopoietic Stem Cells

The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...
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Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...

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Related Experiment Video

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Dissection of Xenopus laevis Neural Crest for in vitro Explant Culture or in vivo Transplantation
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Published on: March 4, 2014

CHD7 cooperates with PBAF to control multipotent neural crest formation.

Ruchi Bajpai1, Denise A Chen, Alvaro Rada-Iglesias

  • 1Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, California 94305, USA.

Nature
|February 5, 2010
PubMed
Summary

CHD7 is crucial for neural crest (NC) cell development, essential for forming craniofacial structures and the nervous system. Mutations in CHD7 cause CHARGE syndrome, highlighting its role in congenital anomalies and cell migration.

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • CHARGE syndrome is a sporadic, autosomal dominant disorder.
  • It is characterized by multiple congenital anomalies.
  • Previous hypotheses suggested neural crest abnormalities, but remained untested.

Purpose of the Study:

  • To investigate the role of CHD7 in neural crest (NC) development.
  • To test the hypothesis that CHARGE syndrome results from abnormal NC development.
  • To elucidate the molecular mechanisms underlying CHD7's function in NC formation and migration.

Main Methods:

  • Studied CHD7 function in human and Xenopus models.
  • Utilized gene knockdown and overexpression techniques in Xenopus embryos.
  • Analyzed CHD7 association with PBAF complex and its binding to regulatory elements (SOX9 enhancer, TWIST1 upstream element) in human NC cells.

Main Results:

  • CHD7 is essential for the formation of multipotent migratory neural crest (NC) cells.
  • CHD7 is required for activating key NC transcriptional circuitry, including Sox9, Twist, and Slug.
  • Knockdown of Chd7 in Xenopus recapitulated CHARGE syndrome features.
  • CHD7 and PBAF cooperate to regulate NC gene expression and cell migration.

Conclusions:

  • CHD7 plays a conserved role in orchestrating NC gene expression programs.
  • This study illuminates the patho-embryology of CHARGE syndrome.
  • CHD7's function extends to regulating cell motility, with implications for broader developmental processes.