Brachyury null mutant-induced defects in juvenile ascidian endodermal organs

Development. 2009 Jan;136(1):35-9. doi: 10.1242/dev.030981. Epub 2008 Nov 19.

Abstract

We report the isolation of a recessive ENU-induced short-tailed mutant in the ascidian Ciona intestinalis that is the product of a premature stop in the brachyury gene. Notochord differentiation and morphogenesis are severely disrupted in the mutant line. At the larval stage, variable degrees of ectopic endoderm staining were observed in the homozygous mutants, indicating that loss of brachyury results in stochastic fate transformation. In post-metamorphosis mutants, a uniform defect in tail resorption was observed, together with variable defects in digestive tract development. Some cells misdirected from the notochord lineage were found to be incorporated into definitive endodermal structures, such as stomach and intestine.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Biomarkers / metabolism
  • Cell Lineage
  • Ciona intestinalis / cytology
  • Ciona intestinalis / growth & development*
  • DNA Mutational Analysis
  • Endoderm / abnormalities*
  • Endoderm / growth & development*
  • Ethylnitrosourea
  • Fetal Proteins / chemistry
  • Fetal Proteins / deficiency*
  • Fetal Proteins / genetics
  • Gastrointestinal Tract / abnormalities
  • Gastrointestinal Tract / growth & development
  • Metamorphosis, Biological
  • Molecular Sequence Data
  • Mutation / genetics*
  • Notochord / cytology
  • Organ Specificity
  • T-Box Domain Proteins / chemistry
  • T-Box Domain Proteins / deficiency*
  • T-Box Domain Proteins / genetics
  • Tail / abnormalities
  • Tail / growth & development

Substances

  • Biomarkers
  • Fetal Proteins
  • T-Box Domain Proteins
  • Brachyury protein
  • Ethylnitrosourea