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The genetic basis of mammalian neurulation

Andrew J Copp1, Nicholas D E Greene, Jennifer N Murdoch

  • 1Neural Development Unit, Institute of Child Health, University College London, London WC1N 1EH, UK. acopp@ich.ucl.ac.uk

Nature Reviews. Genetics
|September 19, 2003
PubMed

Insights

Mutant mouse genes reveal crucial molecular pathways for neural tube development. Studying these genetic models aids understanding of folic acid

Area of Science:

  • Developmental biology
  • Genetics
  • Neuroscience

Background:

  • Neurulation, the process of neural tube formation, is critical for embryonic development.
  • Over 80 mutant mouse genes are known to disrupt neurulation, offering insights into developmental mechanisms.
  • Understanding these disruptions is key to identifying causes of neural tube defects.

Purpose of the Study:

  • To analyze the underlying developmental mechanisms of neurulation using mutant mouse models.
  • To identify molecular pathways essential for normal neural tube closure and development.
  • To explore the role of folic acid in preventing neural tube defects and developing new therapies.

Main Methods:

  • Analysis of over 80 mutant mouse genes affecting neurulation.
  • Investigation of molecular pathways involved in neural tube closure and neural plate bending.
  • Utilizing mutant mice to study folic acid's preventative mechanisms against neural tube defects.

Main Results:

  • Identification of the planar cell-polarity pathway as crucial for initiating neural tube closure.
  • Identification of the sonic hedgehog signalling pathway as essential for regulating neural plate bending.
  • Mutant mouse models provide a platform for studying folic acid's role in preventing neural tube defects.

Conclusions:

  • Mutant mouse genes are invaluable tools for dissecting neurulation mechanisms.
  • Planar cell-polarity and sonic hedgehog pathways are key molecular regulators of neurulation.
  • Further research with mutant mice can lead to novel therapies for neural tube defects, including folate-resistant types.

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