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Related Experiment Videos

lessen encodes a zebrafish trap100 required for enteric nervous system development.

Jacy Pietsch1, Jean-Marie Delalande, Brett Jakaitis

  • 1Department of Biology, Emory University, Rollins Research Center, Atlanta, GA 30322, USA.

Development (Cambridge, England)
|January 7, 2006
PubMed
Summary

The zebrafish lessen (lsn) mutation disrupts Trap100, a key gene for enteric nervous system (ENS) development. This gene is crucial for the proliferation of ENS precursors, not their initial formation or migration.

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Area of Science:

  • Developmental biology
  • Neuroscience
  • Genetics

Background:

  • The enteric nervous system (ENS) is vital for gut function and originates from the vagal neural crest.
  • Understanding the genetic regulation of ENS development is crucial for identifying developmental disorders.

Purpose of the Study:

  • To identify genes essential for vertebrate enteric nervous system (ENS) formation using a zebrafish genetic screen.
  • To elucidate the function of the identified gene, Trap100, in ENS development.

Main Methods:

  • Conducted a genetic screen in zebrafish to isolate mutations affecting ENS development.
  • Characterized the 'lessen' (lsn) mutation and identified it as a loss-of-function mutation in the trap100 gene.
  • Utilized antisense-mediated knockdown, neural crest marker analysis, phosphohistone H3 immunocytochemistry, and cell transplantation studies.

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Main Results:

  • The lsn mutation causes a significant reduction in ENS neurons and defects in cranial neural crest derivatives.
  • lsn encodes zebrafish Trap100, a subunit of the TRAP/mediator transcriptional complex, and its loss-of-function leads to ENS defects.
  • trap100 knockdown phenocopies the lsn mutation, confirming its role.
  • Neural crest specification and migration are unaffected, but ENS precursor proliferation is reduced in lsn mutants.
  • Trap100 acts cell-autonomously in the pharyngeal mesendoderm and secondarily affects neural crest-derived cartilages.
  • Endoderm is essential for ENS development.

Conclusions:

  • lsn/trap100 is not required for the initial specification or migration of cranial neural crest cells.
  • lsn/trap100 is essential for the later proliferation of enteric nervous system precursors within the intestine.
  • This study highlights the critical role of Trap100 in ENS development and provides insights into the genetic control of neural crest derivatives.