QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online 5 January 2006
doi: 10.1242/dev.02215

This Article Figures Only Full Text Full Text (PDF) Supplementary Material All Versions of this Article: dev.02215v1 133/3/395    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pietsch, J. Articles by Shepherd, I. T. Search for Related Content PubMed PubMed Citation Articles by Pietsch, J. Articles by Shepherd, I. T. Social Bookmarking                         What's this?

lessen encodes a zebrafish trap100 required for enteric nervous system development

¹ Department of Biology, Emory University, Rollins Research Center, 1510 Clifton Road, Atlanta GA 30322, USA.
² Department of Developmental Biology, Stanford University School of Medicine, Stanford CA 94305, USA.
³ Department of Biological Structure, University of Washington, Box 357420, Seattle WA 98195, USA.

^* Author for correspondence (e-mail: ishephe{at}emory.edu)

Accepted 21 November 2005

The zebrafish enteric nervous system (ENS), like those of all other vertebrate species, is principally derived from the vagal neural crest. The developmental controls that govern the specification and patterning of the ENS are not well understood. To identify genes required for the formation of the vertebrate ENS, we preformed a genetic screen in zebrafish. We isolated the lessen (lsn) mutation that has a significant reduction in the number of ENS neurons as well as defects in other cranial neural crest derived structures. We show that the lsn gene encodes a zebrafish orthologue of Trap100, one of the subunits of the TRAP/mediator transcriptional regulation complex. A point mutation in trap100 causes a premature stop codon that truncates the protein, causing a loss of function. Antisense-mediated knockdown of trap100 causes an identical phenotype to lsn. During development trap100 is expressed in a dynamic tissue-specific expression pattern consistent with its function in ENS and jaw cartilage development. Analysis of neural crest markers revealed that the initial specification and migration of the neural crest is unaffected in lsn mutants. Phosphohistone H3 immunocytochemistry revealed that there is a significant reduction in proliferation of ENS precursors in lsn mutants. Using cell transplantation studies, we demonstrate that lsn/trap100 acts cell autonomously in the pharyngeal mesendoderm and influences the development of neural crest derived cartilages secondarily. Furthermore, we show that endoderm is essential for ENS development. These studies demonstrate that lsn/trap100 is not required for initial steps of cranial neural crest development and migration, but is essential for later proliferation of ENS precursors in the intestine.

Key words: Neural crest, Zebrafish, Craniofacial, ENS development, lessen (lsn), trap100 (thrap4), Proliferation

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				X. Wang, N. Yang, E. Uno, R. G. Roeder, and S. Guo A subunit of the mediator complex regulates vertebrate neuronal development PNAS, November 14, 2006; 103(46): 17284 - 17289. [Abstract] [Full Text] [PDF]

				K. Durr, J. Holzschuh, A. Filippi, A.-K. Ettl, S. Ryu, I. T. Shepherd, and W. Driever Differential Roles of Transcriptional Mediator Complex Subunits Crsp34/Med27, Crsp150/Med14 and Trap100/Med24 During Zebrafish Retinal Development Genetics, October 1, 2006; 174(2): 693 - 705. [Abstract] [Full Text] [PDF]