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Related Experiment Videos

All-or-none craniorachischisis in Loop-tail mutant mouse chimeras.

T S Musci1, R J Mullen

  • 1Department of Anatomy, University of Utah, School of Medicine, Salt Lake City 84132.

Development (Cambridge, England)
|September 1, 1990
PubMed
Summary

Chimeric mice with Loop-tail (Lp) mutations showed that normal cells can rescue mutant phenotypes, while mutant cells can cause full defects. This suggests a threshold mechanism for neural tube closure in Lp mutants.

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Area of Science:

  • Developmental biology
  • Genetics
  • Teratology

Background:

  • The Loop-tail (Lp) mouse mutant exhibits craniorachischisis, a severe neural tube defect.
  • Understanding the genetic and cellular basis of neural tube defects is crucial for developmental biology.

Purpose of the Study:

  • To investigate the cellular interactions and phenotypic expression in Loop-tail (Lp) mutant mouse chimeras.
  • To determine if genetic mosaicism can rescue or modify the craniorachischisis phenotype.

Main Methods:

  • Generation of experimental chimeric mice by mixing wild-type and Loop-tail (Lp) mutant cells.
  • Analysis of chimeras through gross examination, progeny testing, and glucose phosphate isomerase (GPI) isozyme analysis.

Main Results:

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  • Chimeras displayed an 'all-or-none' phenotype; some were normal despite mutant cells, while others showed full craniorachischisis even with significant wild-type cell contribution.
  • Normal phenotype expression occurred in the presence of mutant cells, and the full mutant phenotype was expressed with up to 50% wild-type cells.

Conclusions:

  • The Loop-tail (Lp) mutant phenotype appears to be regulated by a threshold mechanism, not solely by the proportion of mutant cells.
  • Cellular interactions and a potential threshold effect, rather than a simple cell-autonomous effect, underlie the defective neurulation in Loop-tail mutants.