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Author Notes:

Correspondence: Iain Shepherd, Department of Biology, Emory University, 1510 Clifton Road, Atlanta GA 30322; Tel #: 404-727-2632, Fax #: 404-727-2880, Email: ishephe@emory.edu

We like to thank Andreas Fritz and Robert Esterberg for helpful discussion and comments on the manuscript.

Subject:

Research Funding:

This work has been supported by the NIH under Grant No. 1R01 DK067285-01A1 awarded to Dr. Iain Shepherd, by the Howard Hughes Medical Institute under Grant No. 52003727 awarded to Meaghann Guyote through the SURE program, and by the SIRE Grant awarded by Emory University to Meaghann Guyote.

Keywords:

  • Zebrafish
  • Enteric Nervous System
  • SIP1
  • Mowat-Wilson Syndrome
  • Neural Crest

Zebrafish sip1a and sip1b are Essential for Normal Axial and Neural Patterning

Tools:

Journal Title:

Developmental Dynamics

Volume:

Volume 237, Number 4

Publisher:

, Pages 1060-1069

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Smad-interacting protein-1 (SIP1) has been implicated in the development of Mowat-Wilson syndrome whose patients exhibit Hirschsprung disease, an aganglionosis of the large intestine, as well as other phenotypes. We have identified and cloned two sip1 orthologues in zebrafish. Both sip1 orthologues are expressed maternally and have dynamic zygotic expression patterns that are temporally and spatially distinct. We have investigated the function of both orthologues using translation and splice-blocking morpholino antisense oligonucleotides. Knockdown of the orthologues causes axial and neural patterning defects consistent with the previously described function of SIP1 as an inhibitor of BMP signaling. In addition, knockdown of both genes leads to a significant reduction/loss of the post-otic cranial neural crest. This results in a subsequent absence of neural crest precursors in the posterior pharyngeal arches and a loss of enteric precursors in the intestine.

Copyright information:

© 2008 Wiley-Liss, Inc.

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