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First published online 19 November 2008
doi: 10.1242/dev.030981

Development 136, 35-39 (2009)
Published by The Company of Biologists 2009
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Research Report

brachyury null mutant-induced defects in juvenile ascidian endodermal organs

Shota Chiba1, Di Jiang1,*, Noriyuki Satoh2 and William C. Smith1,{dagger}

1 Department of Molecular, Cell and Developmental Biology, University of California Santa Barbara, Santa Barbara, CA 93106, USA.
2 Department of Zoology, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, 606-8502, Japan.

{dagger} Author for correspondence (e-mail: w_smith{at}lifesci.ucsb.edu)

Accepted 28 October 2008

SUMMARY

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.

Key words: Notochord, Endoderm, Metamorphosis, Ascidian, Ciona intestinalis


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© The Company of Biologists Ltd 2009